苯丙胺:修订间差异

维基百科,自由的百科全书
删除的内容 添加的内容
It's gonna be awesome留言 | 贡献
It's gonna be awesome留言 | 贡献
无编辑摘要
第278行: 第278行:
|group="sources"}}
|group="sources"}}


==用途==
==醫療用途==

===醫療===
{{see also|注意力不足過動症#醫藥治療}}
{{see also|注意力不足過動症#醫藥治療}}
安非他命是用來治療[[注意力不足過動症]](ADHD)、[[嗜睡症]](一種睡眠疾病)、和[[肥胖症]]。有時候安非他命會以{{tsl|en|off-label use|仿單標示外使用}}的方式處方來治療{{tsl|en|treatment-resistant depressiondepression|頑固性憂鬱症}}及'''頑固性強迫症'''<ref name="Amph Uses" /><ref name="Adderall IR">{{cite web
安非他命是用來治療[[注意力不足過動症]](ADHD)、[[嗜睡症]](一種睡眠疾病)、和[[肥胖症]]。有時候安非他命會以{{tsl|en|off-label use|仿單標示外使用}}的方式處方來治療{{tsl|en|treatment-resistant depressiondepression|頑固性憂鬱症}}及'''頑固性強迫症'''<ref name="Amph Uses" /><ref name="Adderall IR">{{cite web
第535行: 第535行:
| quote = }}</ref>
| quote = }}</ref>


In 2015, a [[systematic review]] and a [[meta-analysis]] of high quality [[clinical trial]]s found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including [[working memory]], long-term [[episodic memory]], [[inhibitory control]], and some aspects of [[Attention#Clinical model|attention]], in normal healthy adults;<ref name="Unambiguous PFC D1 A2">{{cite journal | vauthors = Spencer RC, Devilbiss DM, Berridge CW | title = The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex | journal = Biol. Psychiatry | volume = 77 | issue = 11 | pages = 940–950 | year = June 2015 | pmid = 25499957 | doi = 10.1016/j.biopsych.2014.09.013 | quote = The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors.&nbsp;... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function).&nbsp;... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.}}</ref><ref name="Cognitive and motivational effects">{{cite journal | vauthors = Ilieva IP, Hook CJ, Farah MJ | title = Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis | journal = J. Cogn. Neurosci. | pages = 1–21 | date = January 2015 | pmid = 25591060 | doi = 10.1162/jocn_a_00776 | quote = Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities.&nbsp;... The results of this meta-analysis&nbsp;... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.}}</ref> these cognition-enhancing effects of amphetamine are known to be partially mediated through the [[indirect agonist|indirect activation]] of both [[dopamine receptor D1|dopamine receptor D<sub>1</sub>]] and [[Alpha-2 adrenergic receptor|adrenoceptor α<sub>2</sub>]] in the [[prefrontal cortex]].<ref name="Malenka_2009" /><ref name="Unambiguous PFC D1 A2" /> A systematic review from 2014 found that low doses of amphetamine also improve [[memory consolidation]], in turn leading to improved [[Recall (memory)|recall of information]].<ref name="Cognition enhancement 2014 systematic review">{{cite journal | vauthors = Bagot KS, Kaminer Y | title = Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review | journal = Addiction | volume = 109 | issue = 4 | pages = 547–557 | date = April 2014 | pmid = 24749160 | pmc = 4471173 | doi = 10.1111/add.12460 | quote = Amphetamine has been shown to improve consolidation of information (0.02&nbsp;≥&nbsp;P&nbsp;≤&nbsp;0.05), leading to improved recall.}}</ref> Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals.<ref name="Malenka_2009" /><ref name="pmid11337538">{{cite journal |vauthors=Devous MD, Trivedi MH, Rush AJ |title=Regional cerebral blood flow response to oral amphetamine challenge in healthy volunteers |journal=J. Nucl. Med. |volume=42 |issue=4 |pages=535–542 |date=April 2001 |pmid=11337538}}</ref> Amphetamine and other ADHD stimulants also improve [[Incentive salience|task saliency]] (motivation to perform a task) and increase [[arousal]] (wakefulness), in turn promoting goal-directed behavior.<ref name="Malenka_2009" /><ref name="Malenka NAcc">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | page = 266 | edition = 2nd | chapter = Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu | quote = Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.}}</ref><ref name="Continuum">{{cite journal |vauthors=Wood S, Sage JR, Shuman T, Anagnostaras SG |title=Psychostimulants and cognition: a continuum of behavioral and cognitive activation |journal=Pharmacol. Rev. |volume=66 |issue=1 |pages=193–221 |date=January 2014 |pmid=24344115 |doi=10.1124/pr.112.007054}}</ref> Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid.<ref name="Malenka_2009">{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | pages = 318, 321 | edition = 2nd | chapter = Chapter 13: Higher Cognitive Function and Behavioral Control | quote = Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD.&nbsp;... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks&nbsp;... through indirect stimulation of dopamine and norepinephrine receptors.&nbsp;...<br />Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention.}}</ref><ref name="Continuum" /><ref name="Test taking aid">{{cite web | work = JS Online | author = Twohey M | date = 26 March 2006 | title = Pills become an addictive study aid | accessdate = 2 December 2007 | url = http://www.jsonline.com/story/index.aspx?id=410902 | archiveurl = https://web.archive.org/web/20070815200239/http://www.jsonline.com/story/index.aspx?id=410902 | archivedate = 15 August 2007}}</ref> Based upon studies of self-reported illicit stimulant use, 5–35% of college students use [[drug diversion|diverted]] ADHD stimulants, which are primarily used for performance enhancement rather than as recreational drugs.<ref name="pmid16999660">{{cite journal |vauthors=Teter CJ, McCabe SE, LaGrange K, Cranford JA, Boyd CJ | title = Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration | journal = Pharmacotherapy | volume = 26 | issue = 10 | pages = 1501–1510 |date=October 2006 | pmid = 16999660 | pmc = 1794223 | doi = 10.1592/phco.26.10.1501 }}</ref><ref name="Diversion prevalence 1">{{cite journal | vauthors = Weyandt LL, Oster DR, Marraccini ME, Gudmundsdottir BG, Munro BA, Zavras BM, Kuhar B | title = Pharmacological interventions for adolescents and adults with ADHD: stimulant and nonstimulant medications and misuse of prescription stimulants | journal = Psychol. Res. Behav. Manag. | volume = 7 | pages = 223–249 | date = September 2014 | pmid = 25228824 | pmc = 4164338 | doi = 10.2147/PRBM.S47013 | quote = misuse of prescription stimulants has become a serious problem on college campuses across the US and has been recently documented in other countries as well.&nbsp;... Indeed, large numbers of students claim to have engaged in the nonmedical use of prescription stimulants, which is reflected in lifetime prevalence rates of prescription stimulant misuse ranging from 5% to nearly 34% of students.}}</ref><ref name="Diversion prevalence 2">{{cite journal | vauthors = Clemow DB, Walker DJ | title = The potential for misuse and abuse of medications in ADHD: a review | journal = Postgrad. Med. | volume = 126 | issue = 5 | pages = 64–81 | date = September 2014 | pmid = 25295651 | doi = 10.3810/pgm.2014.09.2801 | quote = Overall, the data suggest that ADHD medication misuse and diversion are common health care problems for stimulant medications, with the prevalence believed to be approximately 5% to 10% of high school students and 5% to 35% of college students, depending on the study.}}</ref> However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control.<ref name="Malenka_2009" /><ref name="Continuum" />


==禁忌==
==禁忌==
第556行: 第555行:
==交互作用==
==交互作用==
==藥學==
==藥學==
===作用===

====Cognitive====
In 2015, a [[systematic review]] and a [[meta-analysis]] of high quality [[clinical trial]]s found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including [[working memory]], long-term [[episodic memory]], [[inhibitory control]], and some aspects of [[Attention#Clinical model|attention]], in normal healthy adults;<ref name="Unambiguous PFC D1 A2">{{cite journal | vauthors = Spencer RC, Devilbiss DM, Berridge CW | title = The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex | journal = Biol. Psychiatry | volume = 77 | issue = 11 | pages = 940–950 | year = June 2015 | pmid = 25499957 | doi = 10.1016/j.biopsych.2014.09.013 | quote = The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors.&nbsp;... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function).&nbsp;... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.}}</ref><ref name="Cognitive and motivational effects">{{cite journal | vauthors = Ilieva IP, Hook CJ, Farah MJ | title = Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis | journal = J. Cogn. Neurosci. | pages = 1–21 | date = January 2015 | pmid = 25591060 | doi = 10.1162/jocn_a_00776 | quote = Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities.&nbsp;... The results of this meta-analysis&nbsp;... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.}}</ref> these cognition-enhancing effects of amphetamine are known to be partially mediated through the [[indirect agonist|indirect activation]] of both [[dopamine receptor D1|dopamine receptor D<sub>1</sub>]] and [[Alpha-2 adrenergic receptor|adrenoceptor α<sub>2</sub>]] in the [[prefrontal cortex]].<ref name="Malenka_2009" /><ref name="Unambiguous PFC D1 A2" /> A systematic review from 2014 found that low doses of amphetamine also improve [[memory consolidation]], in turn leading to improved [[Recall (memory)|recall of information]].<ref name="Cognition enhancement 2014 systematic review">{{cite journal | vauthors = Bagot KS, Kaminer Y | title = Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review | journal = Addiction | volume = 109 | issue = 4 | pages = 547–557 | date = April 2014 | pmid = 24749160 | pmc = 4471173 | doi = 10.1111/add.12460 | quote = Amphetamine has been shown to improve consolidation of information (0.02&nbsp;≥&nbsp;P&nbsp;≤&nbsp;0.05), leading to improved recall.}}</ref> Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals.<ref name="Malenka_2009" /><ref name="pmid11337538">{{cite journal |vauthors=Devous MD, Trivedi MH, Rush AJ |title=Regional cerebral blood flow response to oral amphetamine challenge in healthy volunteers |journal=J. Nucl. Med. |volume=42 |issue=4 |pages=535–542 |date=April 2001 |pmid=11337538}}</ref> Amphetamine and other ADHD stimulants also improve [[Incentive salience|task saliency]] (motivation to perform a task) and increase [[arousal]] (wakefulness), in turn promoting goal-directed behavior.<ref name="Malenka_2009" /><ref name="Malenka NAcc">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | page = 266 | edition = 2nd | chapter = Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu | quote = Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.}}</ref><ref name="Continuum">{{cite journal |vauthors=Wood S, Sage JR, Shuman T, Anagnostaras SG |title=Psychostimulants and cognition: a continuum of behavioral and cognitive activation |journal=Pharmacol. Rev. |volume=66 |issue=1 |pages=193–221 |date=January 2014 |pmid=24344115 |doi=10.1124/pr.112.007054}}</ref> Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid.<ref name="Malenka_2009">{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | pages = 318, 321 | edition = 2nd | chapter = Chapter 13: Higher Cognitive Function and Behavioral Control | quote = Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD.&nbsp;... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks&nbsp;... through indirect stimulation of dopamine and norepinephrine receptors.&nbsp;...<br />Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention.}}</ref><ref name="Continuum" /><ref name="Test taking aid">{{cite web | work = JS Online | author = Twohey M | date = 26 March 2006 | title = Pills become an addictive study aid | accessdate = 2 December 2007 | url = http://www.jsonline.com/story/index.aspx?id=410902 | archiveurl = https://web.archive.org/web/20070815200239/http://www.jsonline.com/story/index.aspx?id=410902 | archivedate = 15 August 2007}}</ref> Based upon studies of self-reported illicit stimulant use, 5–35% of college students use [[drug diversion|diverted]] ADHD stimulants, which are primarily used for performance enhancement rather than as recreational drugs.<ref name="pmid16999660">{{cite journal |vauthors=Teter CJ, McCabe SE, LaGrange K, Cranford JA, Boyd CJ | title = Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration | journal = Pharmacotherapy | volume = 26 | issue = 10 | pages = 1501–1510 |date=October 2006 | pmid = 16999660 | pmc = 1794223 | doi = 10.1592/phco.26.10.1501 }}</ref><ref name="Diversion prevalence 1">{{cite journal | vauthors = Weyandt LL, Oster DR, Marraccini ME, Gudmundsdottir BG, Munro BA, Zavras BM, Kuhar B | title = Pharmacological interventions for adolescents and adults with ADHD: stimulant and nonstimulant medications and misuse of prescription stimulants | journal = Psychol. Res. Behav. Manag. | volume = 7 | pages = 223–249 | date = September 2014 | pmid = 25228824 | pmc = 4164338 | doi = 10.2147/PRBM.S47013 | quote = misuse of prescription stimulants has become a serious problem on college campuses across the US and has been recently documented in other countries as well.&nbsp;... Indeed, large numbers of students claim to have engaged in the nonmedical use of prescription stimulants, which is reflected in lifetime prevalence rates of prescription stimulant misuse ranging from 5% to nearly 34% of students.}}</ref><ref name="Diversion prevalence 2">{{cite journal | vauthors = Clemow DB, Walker DJ | title = The potential for misuse and abuse of medications in ADHD: a review | journal = Postgrad. Med. | volume = 126 | issue = 5 | pages = 64–81 | date = September 2014 | pmid = 25295651 | doi = 10.3810/pgm.2014.09.2801 | quote = Overall, the data suggest that ADHD medication misuse and diversion are common health care problems for stimulant medications, with the prevalence believed to be approximately 5% to 10% of high school students and 5% to 35% of college students, depending on the study.}}</ref> However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control.<ref name="Malenka_2009" /><ref name="Continuum" />
====physical====
Amphetamine is used by some athletes for its psychological and [[ergogenic aid|athletic performance-enhancing effects]], such as increased endurance and alertness;<ref name="Ergogenics">{{cite journal |vauthors=Liddle DG, Connor DJ | title = Nutritional supplements and ergogenic AIDS | journal = Prim. Care | volume = 40 | issue = 2 | pages = 487–505 |date=June 2013 | pmid = 23668655 | doi = 10.1016/j.pop.2013.02.009 |quote= Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training&nbsp;...<br />Physiologic and performance effects<br />{{•}}Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake, leading to central nervous system (CNS) stimulation<br />{{•}}Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40<br />{{•}}Improved reaction time<br />{{•}}Increased muscle strength and delayed muscle fatigue<br />{{•}}Increased acceleration<br />{{•}}Increased alertness and attention to task}}</ref><ref name="Westfall" /> however, non-medical amphetamine use is prohibited at sporting events that are regulated by collegiate, national, and international anti-doping agencies.<ref name="NCAA">{{cite web |date=January 2012 | author=Bracken NM | title=National Study of Substance Use Trends Among NCAA College Student-Athletes | url=http://www.ncaapublications.com/productdownloads/SAHS09.pdf | work=NCAA Publications | publisher = National Collegiate Athletic Association | accessdate=8 October 2013}}</ref><ref name="WADA & AD regulation">{{cite journal | author = Docherty JR | title = Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA) | journal = Br. J. Pharmacol. | volume = 154 | issue = 3 | pages = 606–622 | date = June 2008 | pmid = 18500382 | pmc = 2439527 | doi = 10.1038/bjp.2008.124}}</ref> In healthy people at oral therapeutic doses, amphetamine has been shown to increase [[physical strength|muscle strength]],<!--Refs:"Ergogenics" & "Ergogenics2"--> acceleration,<!--Refs:"Ergogenics" & "Ergogenics2"--> athletic performance in [[anaerobic exercise|anaerobic conditions]],<!--Refs:"Ergogenics" & "Ergogenics2"--> and [[endurance]] (i.e., it delays the onset of [[fatigue (medical)|fatigue]]),<!--Refs:"Ergogenics" & "Ergogenics2" & "Roelands_2013"--> while improving [[mental chronometry|reaction time]].<ref name="Ergogenics" /><ref name="Ergogenics2" /><ref name="Roelands_2013" /> Amphetamine improves endurance and reaction time primarily through [[Reuptake inhibitor|reuptake inhibition]] and [[Releasing agent|effluxion]] of dopamine in the central nervous system.<ref name="Ergogenics2" /><ref name="Roelands_2013">{{cite journal |vauthors=Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R | title = Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing | journal = Sports Med. | volume = 43 | issue = 5 | pages = 301–311 |date=May 2013 | pmid = 23456493 | doi = 10.1007/s40279-013-0030-4 | quote = In high-ambient temperatures, dopaminergic manipulations clearly improve performance. The distribution of the power output reveals that after dopamine reuptake inhibition, subjects are able to maintain a higher power output compared with placebo.&nbsp;... Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is ‘off-limits’ in a normal (placebo) situation.}}</ref><ref name="Amph-DA reaction time">{{cite journal |vauthors=Parker KL, Lamichhane D, Caetano MS, Narayanan NS | title = Executive dysfunction in Parkinson's disease and timing deficits | journal = Front. Integr. Neurosci. | volume = 7 | page = 75 | date = October 2013 | pmid = 24198770 | pmc = 3813949 | doi = 10.3389/fnint.2013.00075 | quote = Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or “clock,” activity. For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing;... Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing. }}</ref> Amphetamine and other dopaminergic drugs also increase power output at fixed [[rating of perceived exertion|levels of perceived exertion]] by overriding a "safety switch" that allows the [[Human body temperature|core temperature limit]] to increase in order to access a reserve capacity that is normally off-limits.<ref name="Roelands_2013" /><ref name="Central mechanisms affecting exertion">{{cite journal | vauthors = Rattray B, Argus C, Martin K, Northey J, Driller M | title = Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance? | journal = Front. Physiol. | volume = 6 | pages = 79 | date = March 2015 | pmid = 25852568 | pmc = 4362407 | doi = 10.3389/fphys.2015.00079 | quote = Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al., 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart, 2009).&nbsp;... Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al., 2008)}}</ref><ref name="Monoamine+drug effects on exercise - fatigue and heat">{{cite journal | vauthors = Roelands B, De Pauw K, Meeusen R | title = Neurophysiological effects of exercise in the heat | journal = Scand. J. Med. Sci. Sports | volume = 25 Suppl 1 | pages = 65–78 | date = June 2015 | pmid = 25943657 | doi = 10.1111/sms.12350 | quote = This indicates that subjects did not feel they were producing more power and consequently more heat. The authors concluded that the “safety switch” or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration (Roelands et al., 2008b). Taken together, these data indicate strong ergogenic effects of an increased DA concentration in the brain, without any change in the perception of effort.}}</ref> At therapeutic doses, the adverse effects of amphetamine do not impede athletic performance;<ref name="Ergogenics" /><ref name="Ergogenics2" /> however, at much higher doses, amphetamine can induce effects that severely impair performance, such as [[rhabdomyolysis|rapid muscle breakdown]] and [[hyperthermia|elevated body temperature]].<ref name="FDA Abuse & OD" /><ref name="FDA Effects" /><ref name="Ergogenics2">{{cite journal |author =Parr JW |title=Attention-deficit hyperactivity disorder and the athlete: new advances and understanding |journal=Clin. Sports Med. |volume=30 |issue=3 |pages=591–610 |date=July 2011 |pmid=21658550 |doi=10.1016/j.csm.2011.03.007 |quote=In 1980, Chandler and Blair<sup>47</sup> showed significant increases in knee extension strength, acceleration, anaerobic capacity, time to exhaustion during exercise, pre-exercise and maximum heart rates, and time to exhaustion during maximal oxygen consumption (VO2 max) testing after administration of 15 mg of dextroamphetamine versus placebo. Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise.}}</ref>
}}</onlyinclude>
===[[藥物效應動力學|藥效動力學]]===
===[[藥物效應動力學|藥效動力學]]===



===[[藥物代謝動力學]]===
===[[藥物代謝動力學]]===

2017年4月6日 (四) 04:09的版本

安非他命(Amfetamine) (INN)
An image of the amphetamine compound
A 3d image of the D-amphetamine compound
臨床資料
读音聆聽i/æmˈfɛtəmn/
其他名稱α-methylphenethylamine
AHFS/Drugs.comamphetamine
核准狀況
依賴性生理依賴英语Physical dependence: 無
心理依賴英语Psychological dependence: 中等
成癮性中等
给药途径醫用: 口服给药, 鼻腔給藥, 靜脈注射[1]
Recreational: 口服给药, 鼻腔給藥, Insufflation (medicine)英语Insufflation (medicine), 栓剂, 靜脈注射
ATC碼
法律規範狀態
法律規範
藥物動力學數據
生物利用度口服 75–100%[2]
血漿蛋白結合率15–40%[3]
药物代谢Amphetamine only:
CYP2D6,[4] Dopamine β-hydroxylase,[13][14][15] Flavin-containing monooxygenase英语Flavin-containing monooxygenase[13][16][17]
代謝產物4-hydroxyamphetamine英语4-hydroxyamphetamine, 4-hydroxynorephedrine英语4-hydroxynorephedrine, 4-hydroxyphenylacetone英语4-hydroxyphenylacetone, 苯甲酸, 馬尿酸, 苯丙醇胺, 苯基丙酮[4][5][6]
藥效起始時間英语Onset of actionIR dosing: 30–60 minutes[7]
XR dosing: 1.5–2 hours[8] [9]
生物半衰期D-amph:9–11 hours[4][10]
L-amph:11–14 hours[4][10]
PH值-dependent: 8–31 hours[11]
作用時間IR dosing: 3–7 hours[8][12]
XR dosing: 12 hours[8]

[9]

[12]
排泄途徑Primarily ;
PH值-dependent range: 1–75%[4]
识别信息
  • (RS)-1-phenylpropan-2-amine
CAS号300-62-9  checkY
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
NIAID ChemDB
PDB配體ID
CompTox Dashboard英语CompTox Chemicals Dashboard (EPA)
ECHA InfoCard100.005.543 編輯維基數據鏈接
化学信息
化学式C9H13N
摩尔质量135.20622 g/mol[18]
3D模型(JSmol英语JSmol
密度0.9±0.1 g/cm3
熔点11.3 °C(52.3 °F) (predicted)[20]
沸点203 °C(397 °F) at 760 毫米汞柱[19]
  • NC(CC1=CC=CC=C1)C
  • InChI=1S/C9H13N/c1-8(10)7-9-5-3-2-4-6-9/h2-6,8H,7,10H2,1H3 checkY
  • Key:KWTSXDURSIMDCE-UHFFFAOYSA-N checkY

安非他命(英文名稱:Amphetamine[note 1]为一种中樞神經興奮劑,用來治療注意力不足過動症嗜睡症、和肥胖症。“Amphetamine”一名擷取自 alphamethylphenethylamine

安非他命於西元1887年被發現,以兩種對映異構體的形式存在[note 2] ,分別是左旋安非他命右旋安非他命


正確來說,安非他命指的是特定的化學物質-外消旋純胺類型態英语free base[24][25],這個物質等同於安非他命的的兩個對映異構體:左旋安非他命右旋安非他命的等比化合物之純胺類型態。 然而,實際上安非他命一詞已被廣泛的用來表示任何由安非他命對映異構體構成的物質或安非他命對映異構體本身。[21][26][25]

歸類為中樞神經興奮劑的藥物:派醋甲酯(methylphenidate)和安非他命(amphetamine)。適度適量地使用它們能提升一個人整體的衝動控制能力(inhibitory control)。[27][28] 同理,中樞神經抑制劑(depressants)(例如:酒精)由於會讓腦中神經傳導物質濃度降低、減少許多大腦區域的活性等,所以可能會造成專注力、神智清醒度等自我管理能力的下降。[29]

在醫療用的劑量範圍內,安非他命能帶來情緒以及執行功能的變化,例如:欣快感性欲的改變、清醒度英语wakefulness的提升、大腦執行功能的進化。安非他命所改變的生理反應包含:減少反應時間、降低疲勞、以及肌耐力的增強。然而,若攝取劑量超越醫療用的劑量範圍過多,將會導致大腦執行功能的受損以及肌肉迅速溶解英语rapid muscle breakfast(rapid muscle breakdown)。 攝取過份超越醫療用劑量範圍的安非他命將產生嚴重的藥物成癮風險。然而長期攝取醫療劑量範圍的安非他命並不會產生上癮的風險。

服用嚴重超出醫療用劑量範圍的安非他命會引起精神疾病(例如:妄想[參 1]、偏執[參 2])。然而長期攝取醫療劑量範圍的安非他命並不會引起上述疾病。

娛樂用劑量[參 3][註 1]遠超過醫療用劑量範圍且伴隨著非常嚴重甚至致命的副作用。 [sources 1]

安非他命可以也曾經被用來治療鼻塞(nasal congestion)和抑鬱

安非他命也被用來提升表現英语performance-enhancing substance、和促進大腦的認知功能及在助興時(非醫療用途情況下)被作為增強性慾[a]、和欣快感促進劑

安非他命在許多國家為合法的處方藥[參 4]。然而,私自散布和囤積安非他命被視為非法行為,因為安非他命被用於非醫療用途的助興可能性極高。[sources 2]

首個藥用安非他命的藥品名稱為Benzedrine。當今藥用安非他命英语#Pharmaceutical products[參 5]以下列幾種形式存在:外消旋安非他命[參 6]Adderall[note 3]。 、dextroamphetamine、或對人體無藥效的前驅藥物體[參 7]lisdexamfetamine

Amphetamine, through activation of a trace amine receptor, increases monoamine and excitatory neurotransmitter activity in the brain, with its most pronounced effects targeting the catecholamine neurotransmitters norepinephrine and dopamine.[sources 3]

Amphetamine belongs to the phenethylamine class. It is also the parent compound of its own structural class, the substituted amphetamines,[note 4] which includes prominent substances such as 安非他酮[參 8], cathinone, MDMA, and methamphetamine. As a member of the phenethylamine class, amphetamine is also chemically related to the naturally occurring trace amine neuromodulators, specifically phenethylamine and {{nowrap|[[N-Methylphenethylamine|N-methylphenethylamine}}, both of which are produced within the human body. Phenethylamine is the parent compound of amphetamine, while N-methylphenethylamine is a positional isomer of amphetamine that differs only in the placement of the methyl group英语methyl group.[sources 4]

醫療用途

安非他命是用來治療注意力不足過動症(ADHD)、嗜睡症(一種睡眠疾病)、和肥胖症。有時候安非他命會以仿單標示外使用的方式處方來治療頑固性憂鬱症英语treatment-resistant depressiondepression頑固性強迫症[1][10] [44] [51]。 在動物試驗中,已知非常高劑量的安非他命會造成某些動物的多巴胺系統英语dopamine receptor和神經系統的受損。[52][53] 但是,在人體試驗中,注意力不足過動症患者在接受安非他命的治療後,則發現安非他命可促進大腦的發育及神經的成長。[54][55][56]

回顧許多核磁共振照影(MRI)的研究後發現,長期以安非他命治療注意力不足過動症患者能顯著降低患者大腦結構及大腦執行功能上的異常。並且優化大腦中數個部位,例如:基底神經節的右尾狀核[54][55][56]


眾多臨床研究的系統性及統合性回顧已確立長期使用安非他命治療注意力不足過動症的療效及安全。[57][58][59]

持續長達兩年的隨機對照試驗[參 9][b]結果顯示:長期使用安非他命治療注意力不足過動症,是有效且安全的。[57][59]

兩個系統性/統合性回顧的結果顯示長期且持續地使用中樞神經興奮劑治療注意力不足過動症能有效地減少注意力不足過動症的核心症狀(核心症狀即為:過動、衝動和分心/無法專心)、增進生活品質英语quality of life、提升學業成就、廣泛地強化大腦的執行功能。[note 5] 這些執行功能分別與下列項目有關:學業、反社會行為、駕駛、藥物濫用、肥胖、職業、日常活動、自尊心、服務使用(例如:學習、職業、健康、財金、和法律等)、社交功能。[58][59]

一篇系統性/統合性回顧標誌了一個重要發現:一個為期九個月的隨機雙盲試驗中,持續以安非他命治療的ADHD患者,其智力商數平均增加4.5單位[註 2],且在專注力、衝動、過動的改善皆呈現持續進步的態勢。[57] 另一篇系統性/統合性回顧則指出:根據迄今為止為時最長的數個臨床追蹤研究[參 10],可以得到一個結論:即便從兒童時期開始以中樞神經興奮劑治療直到老年,中樞神經興奮劑都能持續有效地控制ADHD的症狀並且減少物質濫用的風險。[59] 研究表明,ADHD與大腦的執行功能受損有關。而這些受損的執行功能分別與大腦中部分的神經傳導系統英语neurostransmitter systems[參 11][60] ;又此部分受損的神經傳導系統和中腦皮質激素英语mesocorticolimbic projection-多巴胺[參 12]的傳導及藍斑核[參 13]前額葉[參 14]中的正腎上腺素[參 15]的傳導相關。[60]

中樞神經興奮劑,例如:methylphenidate和安非他命對於治療ADHD都是有效的,因為中樞神經興奮劑刺激了上述神經系統中的神經傳導物質活動。[30][60] [61]

至少超過80%的ADHD患者在使用中樞神經興奮劑治療後,其ADHD的症狀可以獲得改善。[62]

使用中樞神經興奮劑治療的ADHD患者相較之下,普遍與同儕及家庭成員的關係較佳並且在學校擁有較好的表現。興奮劑能使ADHD患者較不易分心、衝動、且擁有較長的專注力時間和範圍。[63] [64]

根據考科藍協作組織[參 16]所提供的文獻回顧結果[note 6]指出:使用中樞神經興奮劑治療的ADHD患者即便其症狀改善,相較於使用非中樞神經興奮劑,仍因副作用而有較高的停藥率。[66] [67]

回顧結果也發現,中樞神經興奮劑並不會惡化抽動綜合症的症狀,例如:妥瑞氏症,除非服用dextroamphetamine[c]的劑量過高才有可能在部分妥瑞氏症合併注意路不足過動症患者身上觀察到抽動綜合症的症狀惡化。[68]

中樞神經興奮劑只要依照醫師指示用藥,都是相當安全的。[69][70][70][71] 中樞神經興奮劑,例如:利他能與專思達,可能導致:心悸、頭痛、胃痛、喪失食慾、失眠、因相對專注而變得冷淡(面無表情)等副作用,因此6歲以下的兒童不適宜服用。(副作用產生與否因人而異) [72]

隨著時間推進與各方的努力,中樞神經興奮劑的相關副作用已可藉由包括但不限於劑量調整、服藥時間、飯前飯後服用、服藥頻率等服藥模式之改變以及改變藥物組合等方式獲得相當程度的減少。[73] [74] [75] [70] [76]


禁忌

According to the International Programme on Chemical Safety (IPCS) and United States Food and Drug Administration (USFDA),[note 7] amphetamine is contraindicated in people with a history of drug abuse,[note 8] cardiovascular disease, severe agitation, or severe anxiety.[78][79] It is also contraindicated in people currently experiencing arteriosclerosis (hardening of the arteries), glaucoma (increased eye pressure), hyperthyroidism (excessive production of thyroid hormone), or moderate to severe hypertension.[78][79][80] People who have experienced allergic reactions to other stimulants in the past or who are taking monoamine oxidase inhibitors (MAOIs) are advised not to take amphetamine,[78][79] although safe concurrent use of amphetamine and monoamine oxidase inhibitors has been documented.[81][82] These agencies also state that anyone with anorexia nervosa, bipolar disorder, depression, hypertension, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics, or Tourette syndrome should monitor their symptoms while taking amphetamine.[78][79] Evidence from human studies indicates that therapeutic amphetamine use does not cause developmental abnormalities in the fetus or newborns (i.e., it is not a human teratogen), but amphetamine abuse does pose risks to the fetus.[79] Amphetamine has also been shown to pass into breast milk, so the IPCS and USFDA advise mothers to avoid breastfeeding when using it.[78][79] Due to the potential for reversible growth impairments,[note 9] the USFDA advises monitoring the height and weight of children and adolescents prescribed an amphetamine pharmaceutical.[78]

副作用

生理

心理

嚴重過量

成癮

依賴和戒斷症狀

交互作用

藥學

作用

Cognitive

In 2015, a systematic review and a meta-analysis of high quality clinical trials found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including working memory, long-term episodic memory, inhibitory control, and some aspects of attention, in normal healthy adults;[27][28] these cognition-enhancing effects of amphetamine are known to be partially mediated through the indirect activation of both dopamine receptor D1 and adrenoceptor α2 in the prefrontal cortex.[30][27] A systematic review from 2014 found that low doses of amphetamine also improve memory consolidation, in turn leading to improved recall of information.[84] Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals.[30][85] Amphetamine and other ADHD stimulants also improve task saliency (motivation to perform a task) and increase arousal (wakefulness), in turn promoting goal-directed behavior.[30][86][87] Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid.[30][87][88] Based upon studies of self-reported illicit stimulant use, 5–35% of college students use diverted ADHD stimulants, which are primarily used for performance enhancement rather than as recreational drugs.[89][90][91] However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control.[30][87]

physical

Amphetamine is used by some athletes for its psychological and athletic performance-enhancing effects, such as increased endurance and alertness;[31][35] however, non-medical amphetamine use is prohibited at sporting events that are regulated by collegiate, national, and international anti-doping agencies.[92][93] In healthy people at oral therapeutic doses, amphetamine has been shown to increase muscle strength, acceleration, athletic performance in anaerobic conditions, and endurance (i.e., it delays the onset of fatigue), while improving reaction time.[31][94][95] Amphetamine improves endurance and reaction time primarily through reuptake inhibition and effluxion of dopamine in the central nervous system.[94][95][96] Amphetamine and other dopaminergic drugs also increase power output at fixed levels of perceived exertion by overriding a "safety switch" that allows the core temperature limit to increase in order to access a reserve capacity that is normally off-limits.[95][97][98] At therapeutic doses, the adverse effects of amphetamine do not impede athletic performance;[31][94] however, at much higher doses, amphetamine can induce effects that severely impair performance, such as rapid muscle breakdown and elevated body temperature.[32][34][94] }}

藥效動力學

藥物代謝動力學

相關的內部生成化合物/混和物(endogenous compound)

歷史、社會與文化

合法狀態與條件

藥品

備註A

  1. ^ 别名有:1-phenylpropan-2-amine (IUPAC name), α-methylbenzeneethanamine, α-methylphenethylamine, amfetamine (International Nonproprietary Name [INN]), β-phenylisopropylamine, desoxynorephedrine, and speed.[18][21][22]
  2. ^ 對映異構體指的是 are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation.[23]Levoamphetamine and dextroamphetamine are also known as L-amph or levamfetamine (INN) and D-amph or dexamfetamine (INN) respectively.[18]
  3. ^ "Adderall" is a 品牌名稱 as opposed to a nonproprietary name; because the latter ("dextroamphetamine sulfate, dextroamphetamine saccharate, amphetamine sulfate, and amphetamine aspartate" [45]) is excessively long, this article exclusively refers to this amphetamine mixture by the brand name.
  4. ^ The term "amphetamines" also refers to a chemical class, but, unlike the class of substituted amphetamines,[13] the "amphetamines" class does not have a standardized definition in academic literature.[25] One of the more restrictive definitions of this class includes only the racemate and enantiomers of amphetamine and methamphetamine.[25] The most general definition of the class encompasses a broad range of pharmacologically and structurally related compounds.[25]
    Due to confusion that may arise from use of the plural form, this article will only use the terms "amphetamine" and "amphetamines" to refer to racemic amphetamine, levoamphetamine, and dextroamphetamine and reserve the term "substituted amphetamines" for its structural class.
  5. ^ The ADHD-related outcome domains with the greatest proportion of significantly improved outcomes from long-term continuous stimulant therapy include academics (~55% of academic outcomes improved), driving (100% of driving outcomes improved), non-medical drug use (47% of addiction-related outcomes improved), obesity (~65% of obesity-related outcomes improved), self esteem (50% of self-esteem outcomes improved), and social function (67% of social function outcomes improved).[58]

    The largest effect sizes for outcome improvements from long-term stimulant therapy occur in the domains involving academics (e.g., grade point average英语grade point average, achievement test scores, length of education, and education level), self-esteem (e.g., self-esteem questionnaire assessments, number of suicide attempts, and suicide rates), and social function (e.g., peer nomination scores, social skills, and quality of peer, family, and romantic relationships).[58]

    Long-term combination therapy for ADHD (i.e., treatment with both a stimulant and behavioral therapy) produces even larger effect sizes for outcome improvements and improves a larger proportion of outcomes across each domain compared to long-term stimulant therapy alone.[58]
  6. ^ Cochrane Collaboration reviews are high quality meta-analytic systematic reviews of randomized controlled trials.[65]
  7. ^ The statements supported by the USFDA come from prescribing information, which is the copyrighted intellectual property of the manufacturer and approved by the USFDA. USFDA contraindications are not necessarily intended to limit medical practice but limit claims by pharmaceutical companies.[77]
  8. ^ According to one review, amphetamine can be prescribed to individuals with a history of abuse provided that appropriate medication controls are employed, such as requiring daily pick-ups of the medication from the prescribing physician.[1]
  9. ^ In individuals who experience sub-normal height and weight gains, a rebound to normal levels is expected to occur if stimulant therapy is briefly interrupted.[57][59][83] The average reduction in final adult height from continuous stimulant therapy over a 3 year period is 2 cm.[83]

備註B

  1. ^ 雖稱為娛樂用劑量,然而實際上卻無法達成娛樂效果,反而將導致嚴重的併發症。
  2. ^ 智力測驗結果與專注力有關,詳見注意力不足過動症#智力

注释

  1. ^ 安非他命乃春藥的其中一種
  2. ^ 又稱為「隨機分配且包含控制組的臨床試驗」,是臨床試驗的一種
  3. ^ 中樞神經興奮劑的一種

英文名稱對照

  1. ^ 英文名稱為:delusions
  2. ^ 英文名稱為:paranoia
  3. ^ 英文名稱為:recreational dose
  4. ^ 英文名稱為:Prescription drug
  5. ^ 英文名稱為:Pharmaceutical amphetamine
  6. ^ 英文名稱為:racemic amphetamine
  7. ^ 英文名稱為:Prodrug
  8. ^ 英文名稱為:Bupropion
  9. ^ 英文名稱為:Randomized controlled trials
  10. ^ 英文名稱為:follow-up studies
  11. ^ 英文名稱為:neurotransmitter systems
  12. ^ 英文名稱為:dopamine
  13. ^ 英文名稱為:locus coeruleus
  14. ^ 英文名稱為:prefrontal cortex
  15. ^ 英文名稱為:nor-epinephrine或nor-adrenaline
  16. ^ 英文名稱為:Cochrane Collaboration

引用

來源

  1. ^ 1.0 1.1 1.2 1.3 1.4 引证错误:没有为名为Amph Uses的参考文献提供内容
  2. ^ 引证错误:没有为名为Drugbank-dexamph的参考文献提供内容
  3. ^ 引证错误:没有为名为Drugbank-amph的参考文献提供内容
  4. ^ 4.0 4.1 4.2 4.3 4.4 引证错误:没有为名为FDA Pharmacokinetics的参考文献提供内容
  5. ^ 引证错误:没有为名为Pubchem Kinetics的参考文献提供内容
  6. ^ 引证错误:没有为名为Metabolites的参考文献提供内容
  7. ^ amphetamine/dextroamphetamine. Medscape. WebMD. Onset of action: 30–60 min  |section-url=被忽略 (帮助); |section=被忽略 (帮助);
  8. ^ 8.0 8.1 8.2 Millichap JG. Chapter 9: Medications for ADHD. Millichap JG (编). Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD 2nd. New York, USA: Springer. 2010: 112. ISBN 9781441913968.
    Table 9.2 Dextroamphetamine formulations of stimulant medication
    Dexedrine [Peak:2–3 h] [Duration:5–6 h] ...
    Adderall [Peak:2–3 h] [Duration:5–7 h]
    Dexedrine spansules [Peak:7–8 h] [Duration:12 h] ...
    Adderall XR [Peak:7–8 h] [Duration:12 h]
    Vyvanse [Peak:3–4 h] [Duration:12 h]
     
  9. ^ 9.0 9.1 Brams M, Mao AR, Doyle RL. Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder. Postgrad. Med. September 2008, 120 (3): 69–88. PMID 18824827. doi:10.3810/pgm.2008.09.1909. 
  10. ^ 10.0 10.1 10.2 10.3 10.4 Adderall IR Prescribing Information (PDF). United States Food and Drug Administration. Teva Pharmaceuticals USA, Inc.: 1–6. October 2015 [18 May 2016]. 
  11. ^ 引证错误:没有为名为pH-dependent half-lives的参考文献提供内容
  12. ^ 12.0 12.1 Mignot EJ. A practical guide to the therapy of narcolepsy and hypersomnia syndromes. Neurotherapeutics. October 2012, 9 (4): 739–752. PMC 3480574可免费查阅. PMID 23065655. doi:10.1007/s13311-012-0150-9. 
  13. ^ 13.0 13.1 13.2 引证错误:没有为名为Substituted amphetamines, FMO, and DBH的参考文献提供内容
  14. ^ 引证错误:没有为名为DBH amph primary的参考文献提供内容
  15. ^ 引证错误:没有为名为DBH 4-HA primary的参考文献提供内容
  16. ^ 引证错误:没有为名为FMO的参考文献提供内容
  17. ^ 引证错误:没有为名为FMO3-Primary的参考文献提供内容
  18. ^ 18.0 18.1 18.2 引证错误:没有为名为PubChem Header的参考文献提供内容
  19. ^ 引证错误:没有为名为Properties的参考文献提供内容
  20. ^ Amphetamine. Chemspider.  |section-url=被忽略 (帮助); |section=被忽略 (帮助);
  21. ^ 21.0 21.1 引证错误:没有为名为DrugBank1的参考文献提供内容
  22. ^ 引证错误:没有为名为Acute amph toxicity的参考文献提供内容
  23. ^ Enantiomer. IUPAC Goldbook. International Union of Pure and Applied Chemistry. [14 March 2014]. doi:10.1351/goldbook.E02069. (原始内容存档于17 March 2013). One of a pair of molecular entities which are mirror images of each other and non-superposable. 
  24. ^ 24.0 24.1 Guidelines on the Use of International Nonproprietary Names (INNS) for Pharmaceutical Substances. World Health Organization. 1997 [1 December 2014]. In principle, INNs are selected only for the active part of the molecule which is usually the base, acid or alcohol. In some cases, however, the active molecules need to be expanded for various reasons, such as formulation purposes, bioavailability or absorption rate. In 1975 the experts designated for the selection of INN decided to adopt a new policy for naming such molecules. In future, names for different salts or esters of the same active substance should differ only with regard to the inactive moiety of the molecule. ... The latter are called modified INNs (INNMs). 
  25. ^ 25.0 25.1 25.2 25.3 25.4 25.5 Yoshida T. Chapter 1: Use and Misuse of Amphetamines: An International Overview. Klee H (编). Amphetamine Misuse: International Perspectives on Current Trends. Amsterdam, Netherlands: Harwood Academic Publishers. 1997: 2 [1 December 2014]. ISBN 9789057020810. Amphetamine, in the singular form, properly applies to the racemate of 2-amino-1-phenylpropane. ... In its broadest context, however, the term [amphetamines] can even embrace a large number of structurally and pharmacologically related substances. 
  26. ^ 26.0 26.1 Amphetamine. Medical Subject Headings. United States National Library of Medicine. [16 December 2013]. 
  27. ^ 27.0 27.1 27.2 Spencer RC, Devilbiss DM, Berridge CW. The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex. Biol. Psychiatry. June 2015, 77 (11): 940–950. PMID 25499957. doi:10.1016/j.biopsych.2014.09.013. The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. ... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation. ... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.  引证错误:带有name属性“Unambiguous PFC D1 A2”的<ref>标签用不同内容定义了多次
  28. ^ 28.0 28.1 Ilieva IP, Hook CJ, Farah MJ. Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis. J. Cogn. Neurosci. January 2015: 1–21. PMID 25591060. doi:10.1162/jocn_a_00776. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ... The results of this meta-analysis ... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.  引证错误:带有name属性“Cognitive and motivational effects”的<ref>标签用不同内容定义了多次
  29. ^ Long-term & Short-term effects, depressants, brand names: Foundation for a drug free work. 
  30. ^ 30.0 30.1 30.2 30.3 30.4 30.5 30.6 30.7 30.8 Malenka RC, Nestler EJ, Hyman SE. Chapter 13: Higher Cognitive Function and Behavioral Control. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 318, 321. ISBN 9780071481274. Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors. ...
    Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention.
     
  31. ^ 31.0 31.1 31.2 31.3 31.4 Liddle DG, Connor DJ. Nutritional supplements and ergogenic AIDS. Prim. Care. June 2013, 40 (2): 487–505. PMID 23668655. doi:10.1016/j.pop.2013.02.009. Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training ...
    Physiologic and performance effects
     · Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake, leading to central nervous system (CNS) stimulation
     · Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40
     · Improved reaction time
     · Increased muscle strength and delayed muscle fatigue
     · Increased acceleration
     · Increased alertness and attention to task
     
  32. ^ 32.0 32.1 32.2 引证错误:没有为名为FDA Abuse & OD的参考文献提供内容
  33. ^ 33.0 33.1 引证错误:没有为名为Libido的参考文献提供内容
  34. ^ 34.0 34.1 引证错误:没有为名为FDA Effects的参考文献提供内容
  35. ^ 35.0 35.1 引证错误:没有为名为Westfall的参考文献提供内容
  36. ^ 引证错误:没有为名为Cochrane的参考文献提供内容
  37. ^ 引证错误:没有为名为Stimulant Misuse的参考文献提供内容
  38. ^ 引证错误:没有为名为NHM-Addiction doses的参考文献提供内容
  39. ^ 引证错误:没有为名为Addiction risk的参考文献提供内容
  40. ^ 引证错误:没有为名为EncycOfPsychopharm的参考文献提供内容
  41. ^ 41.0 41.1 引证错误:没有为名为Benzedrine的参考文献提供内容
  42. ^ 引证错误:没有为名为UN Convention的参考文献提供内容
  43. ^ 引证错误:没有为名为Nonmedical的参考文献提供内容
  44. ^ 44.0 44.1 44.2 引证错误:没有为名为Evekeo的参考文献提供内容
  45. ^ National Drug Code Amphetamine Search Results. National Drug Code Directory. United States Food and Drug Administration. [16 December 2013]. (原始内容存档于16 December 2013). 
  46. ^ 引证错误:没有为名为Miller的参考文献提供内容
  47. ^ 引证错误:没有为名为Miller+Grandy 2016的参考文献提供内容
  48. ^ 引证错误:没有为名为Trace Amines的参考文献提供内容
  49. ^ Amphetamine. European Monitoring Centre for Drugs and Drug Addiction. [19 October 2013]. 
  50. ^ 引证错误:没有为名为Amphetamine - a substituted amphetamine的参考文献提供内容
  51. ^ Obsessive compulsive disorder (OCD). NHS Choice. 2016-09-28 [2017-04-04]. 
  52. ^ 引证错误:没有为名为pmid22392347的参考文献提供内容
  53. ^ Berman S, O'Neill J, Fears S, Bartzokis G, London ED. Abuse of amphetamines and structural abnormalities in the brain. Ann. N. Y. Acad. Sci. October 2008, 1141: 195–220. PMC 2769923可免费查阅. PMID 18991959. doi:10.1196/annals.1441.031. 
  54. ^ 54.0 54.1 Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K. Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects. JAMA Psychiatry. February 2013, 70 (2): 185–198. PMID 23247506. doi:10.1001/jamapsychiatry.2013.277. 
  55. ^ 55.0 55.1 Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J. Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies. J. Clin. Psychiatry. September 2013, 74 (9): 902–917. PMC 3801446可免费查阅. PMID 24107764. doi:10.4088/JCP.12r08287. 
  56. ^ 56.0 56.1 Frodl T, Skokauskas N. Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.. Acta psychiatrica Scand. February 2012, 125 (2): 114–126. PMID 22118249. doi:10.1111/j.1600-0447.2011.01786.x. Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure. 
  57. ^ 57.0 57.1 57.2 57.3 Millichap JG. Chapter 9: Medications for ADHD. Millichap JG (编). Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD 2nd. New York, USA: Springer. 2010: 121–123, 125–127. ISBN 9781441913968. Ongoing research has provided answers to many of the parents’ concerns, and has confirmed the effectiveness and safety of the long-term use of medication. 
  58. ^ 58.0 58.1 58.2 58.3 58.4 Arnold LE, Hodgkins P, Caci H, Kahle J, Young S. Effect of treatment modality on long-term outcomes in attention-deficit/hyperactivity disorder: a systematic review. PLoS ONE. February 2015, 10 (2): e0116407. PMC 4340791可免费查阅. PMID 25714373. doi:10.1371/journal.pone.0116407. The highest proportion of improved outcomes was reported with combination treatment (83% of outcomes). Among significantly improved outcomes, the largest effect sizes were found for combination treatment. The greatest improvements were associated with academic, self-esteem, or social function outcomes. 
    Figure 3: Treatment benefit by treatment type and outcome group
  59. ^ 59.0 59.1 59.2 59.3 59.4 Huang YS, Tsai MH. Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge. CNS Drugs. July 2011, 25 (7): 539–554. PMID 21699268. doi:10.2165/11589380-000000000-00000. Recent studies have demonstrated that stimulants, along with the non-stimulants atomoxetine and extended-release guanfacine, are continuously effective for more than 2-year treatment periods with few and tolerable adverse effects. The effectiveness of long-term therapy includes not only the core symptoms of ADHD, but also improved quality of life and academic achievements. The most concerning short-term adverse effects of stimulants, such as elevated blood pressure and heart rate, waned in long-term follow-up studies. ... In the longest follow-up study (of more than 10 years), lifetime stimulant treatment for ADHD was effective and protective against the development of adverse psychiatric disorders. 
  60. ^ 60.0 60.1 60.2 Malenka RC, Nestler EJ, Hyman SE. Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 154–157. ISBN 9780071481274. 
  61. ^ Bidwell LC, McClernon FJ, Kollins SH. Cognitive enhancers for the treatment of ADHD. Pharmacol. Biochem. Behav. August 2011, 99 (2): 262–274. PMC 3353150可免费查阅. PMID 21596055. doi:10.1016/j.pbb.2011.05.002. 
  62. ^ Parker J, Wales G, Chalhoub N, Harpin V. The long-term outcomes of interventions for the management of attention-deficit hyperactivity disorder in children and adolescents: a systematic review of randomized controlled trials. Psychol. Res. Behav. Manag. (systematic review (secondary source)). September 2013, 6: 87–99. PMC 3785407可免费查阅. PMID 24082796. doi:10.2147/PRBM.S49114. Only one paper53 examining outcomes beyond 36 months met the review criteria. ... There is high level evidence suggesting that pharmacological treatment can have a major beneficial effect on the core symptoms of ADHD (hyperactivity, inattention, and impulsivity) in approximately 80% of cases compared with placebo controls, in the short term. 
  63. ^ Millichap JG. Chapter 9: Medications for ADHD. Millichap JG (编). Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD 2nd. New York, USA: Springer. 2010: 111–113. ISBN 9781441913968. 
  64. ^ Stimulants for Attention Deficit Hyperactivity Disorder. WebMD. Healthwise. 12 April 2010 [12 November 2013]. 
  65. ^ Scholten RJ, Clarke M, Hetherington J. The Cochrane Collaboration. Eur. J. Clin. Nutr. August 2005,. 59 Suppl 1: S147–S149; discussion S195–S196. PMID 16052183. doi:10.1038/sj.ejcn.1602188. 
  66. ^ Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M. Castells X , 编. Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults. Cochrane Database Syst. Rev. June 2011, (6): CD007813. PMID 21678370. doi:10.1002/14651858.CD007813.pub2. 
  67. ^ Punja S, Shamseer L, Hartling L, Urichuk L, Vandermeer B, Nikles J, Vohra S. Amphetamines for attention deficit hyperactivity disorder (ADHD) in children and adolescents. Cochrane Database Syst. Rev. February 2016, 2: CD009996. PMID 26844979. doi:10.1002/14651858.CD009996.pub2. 
  68. ^ Pringsheim T, Steeves T. Pringsheim T , 编. Pharmacological treatment for Attention Deficit Hyperactivity Disorder (ADHD) in children with comorbid tic disorders. Cochrane Database Syst. Rev. April 2011, (4): CD007990. PMID 21491404. doi:10.1002/14651858.CD007990.pub2. 
  69. ^ 引证错误:没有为名为medlineplus1的参考文献提供内容
  70. ^ 70.0 70.1 70.2 Abuse, National Institute on Drug. Stimulant ADHD Medications: Methylphenidate and Amphetamines. 
  71. ^ Choices, N. H. S. What is a controlled medicine (drug)? - Health questions - NHS Choices. 2016-12-12. 
  72. ^ Methylphenidate. Home of MedlinePlus → Drugs, Herbs and Supplements → Methylphenidate Methylphenidate pronounced as (meth il fen' i date). 2016-02-15 [February twenty seventh, 2017]. 
  73. ^ Combining medications could offer better results for ADHD patients. Science News. Elsevier. 2016-08-01 [January 2017]. (原始内容存档于August 2016). "Three studies to be published in the August 2016 issue of the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP) report that combining two standard medications could lead to greater clinical improvements for children with attention-deficit/hyperactivity disorder (ADHD) than either ADHD therapy alone.", August, 2016 
  74. ^ Adults with ADHD. MedlinePlus the Magazine 9. 8600 Rockville Pike • Bethesda, MD 20894, United States of America: NATIONAL LIBRARY OF MEDICINE at the NATIONAL INSTITUTES OF HEALTH. Spring 2014: 19. ISSN 1937-4712 (美国英语). 
  75. ^ Attention deficit hyperactivity disorder. Home → Medical Encyclopedia → Attention deficit hyperactivity disorder. NATIONAL LIBRARY OF MEDICINE at the NATIONAL INSTITUTES OF HEALTH. 2016-05-25 [February twenty seventh, 2017.]. 
  76. ^ All Disorders. National Institute of Neurological Disorders and Stroke. [February twenty seventh, 2017]. 
  77. ^ Kessler S. Drug therapy in attention-deficit hyperactivity disorder. South. Med. J. January 1996, 89 (1): 33–38. PMID 8545689. doi:10.1097/00007611-199601000-00005. statements on package inserts are not intended to limit medical practice. Rather they are intended to limit claims by pharmaceutical companies. ... the FDA asserts explicitly, and the courts have upheld that clinical decisions are to be made by physicians and patients in individual situations. 
  78. ^ 78.0 78.1 78.2 78.3 78.4 78.5 引证错误:没有为名为FDA Contra Warnings的参考文献提供内容
  79. ^ 79.0 79.1 79.2 79.3 79.4 79.5 Heedes G, Ailakis J. Amphetamine (PIM 934). INCHEM. International Programme on Chemical Safety. [24 June 2014]. 
  80. ^ 引证错误:没有为名为Dexedrine FDA的参考文献提供内容
  81. ^ Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J. Clin. Psychiatry. November 2004, 65 (11): 1520–1524. PMID 15554766. doi:10.4088/jcp.v65n1113. 
  82. ^ Stewart JW, Deliyannides DA, McGrath PJ. How treatable is refractory depression?. J. Affect. Disord. June 2014, 167: 148–152. PMID 24972362. doi:10.1016/j.jad.2014.05.047. 
  83. ^ 83.0 83.1 引证错误:没有为名为pmid18295156的参考文献提供内容
  84. ^ Bagot KS, Kaminer Y. Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review. Addiction. April 2014, 109 (4): 547–557. PMC 4471173可免费查阅. PMID 24749160. doi:10.1111/add.12460. Amphetamine has been shown to improve consolidation of information (0.02 ≥ P ≤ 0.05), leading to improved recall. 
  85. ^ Devous MD, Trivedi MH, Rush AJ. Regional cerebral blood flow response to oral amphetamine challenge in healthy volunteers. J. Nucl. Med. April 2001, 42 (4): 535–542. PMID 11337538. 
  86. ^ Malenka RC, Nestler EJ, Hyman SE. Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York, USA: McGraw-Hill Medical. 2009: 266. ISBN 9780071481274. Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. 
  87. ^ 87.0 87.1 87.2 Wood S, Sage JR, Shuman T, Anagnostaras SG. Psychostimulants and cognition: a continuum of behavioral and cognitive activation. Pharmacol. Rev. January 2014, 66 (1): 193–221. PMID 24344115. doi:10.1124/pr.112.007054. 
  88. ^ Twohey M. Pills become an addictive study aid. JS Online. 26 March 2006 [2 December 2007]. (原始内容存档于15 August 2007). 
  89. ^ Teter CJ, McCabe SE, LaGrange K, Cranford JA, Boyd CJ. Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration. Pharmacotherapy. October 2006, 26 (10): 1501–1510. PMC 1794223可免费查阅. PMID 16999660. doi:10.1592/phco.26.10.1501. 
  90. ^ Weyandt LL, Oster DR, Marraccini ME, Gudmundsdottir BG, Munro BA, Zavras BM, Kuhar B. Pharmacological interventions for adolescents and adults with ADHD: stimulant and nonstimulant medications and misuse of prescription stimulants. Psychol. Res. Behav. Manag. September 2014, 7: 223–249. PMC 4164338可免费查阅. PMID 25228824. doi:10.2147/PRBM.S47013. misuse of prescription stimulants has become a serious problem on college campuses across the US and has been recently documented in other countries as well. ... Indeed, large numbers of students claim to have engaged in the nonmedical use of prescription stimulants, which is reflected in lifetime prevalence rates of prescription stimulant misuse ranging from 5% to nearly 34% of students. 
  91. ^ Clemow DB, Walker DJ. The potential for misuse and abuse of medications in ADHD: a review. Postgrad. Med. September 2014, 126 (5): 64–81. PMID 25295651. doi:10.3810/pgm.2014.09.2801. Overall, the data suggest that ADHD medication misuse and diversion are common health care problems for stimulant medications, with the prevalence believed to be approximately 5% to 10% of high school students and 5% to 35% of college students, depending on the study. 
  92. ^ Bracken NM. National Study of Substance Use Trends Among NCAA College Student-Athletes (PDF). NCAA Publications. National Collegiate Athletic Association. January 2012 [8 October 2013]. 
  93. ^ Docherty JR. Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA). Br. J. Pharmacol. June 2008, 154 (3): 606–622. PMC 2439527可免费查阅. PMID 18500382. doi:10.1038/bjp.2008.124. 
  94. ^ 94.0 94.1 94.2 94.3 Parr JW. Attention-deficit hyperactivity disorder and the athlete: new advances and understanding. Clin. Sports Med. July 2011, 30 (3): 591–610. PMID 21658550. doi:10.1016/j.csm.2011.03.007. In 1980, Chandler and Blair47 showed significant increases in knee extension strength, acceleration, anaerobic capacity, time to exhaustion during exercise, pre-exercise and maximum heart rates, and time to exhaustion during maximal oxygen consumption (VO2 max) testing after administration of 15 mg of dextroamphetamine versus placebo. Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise. 
  95. ^ 95.0 95.1 95.2 Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R. Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing. Sports Med. May 2013, 43 (5): 301–311. PMID 23456493. doi:10.1007/s40279-013-0030-4. In high-ambient temperatures, dopaminergic manipulations clearly improve performance. The distribution of the power output reveals that after dopamine reuptake inhibition, subjects are able to maintain a higher power output compared with placebo. ... Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is ‘off-limits’ in a normal (placebo) situation. 
  96. ^ Parker KL, Lamichhane D, Caetano MS, Narayanan NS. Executive dysfunction in Parkinson's disease and timing deficits. Front. Integr. Neurosci. October 2013, 7: 75. PMC 3813949可免费查阅. PMID 24198770. doi:10.3389/fnint.2013.00075. Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or “clock,” activity. For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing;... Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing. 
  97. ^ Rattray B, Argus C, Martin K, Northey J, Driller M. Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?. Front. Physiol. March 2015, 6: 79. PMC 4362407可免费查阅. PMID 25852568. doi:10.3389/fphys.2015.00079. Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al., 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart, 2009). ... Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al., 2008) 
  98. ^ Roelands B, De Pauw K, Meeusen R. Neurophysiological effects of exercise in the heat. Scand. J. Med. Sci. Sports. June 2015,. 25 Suppl 1: 65–78. PMID 25943657. doi:10.1111/sms.12350. This indicates that subjects did not feel they were producing more power and consequently more heat. The authors concluded that the “safety switch” or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration (Roelands et al., 2008b). Taken together, these data indicate strong ergogenic effects of an increased DA concentration in the brain, without any change in the perception of effort. 

外部連結

Template:Phenethylamines