Cocaine
Subclass of | ester, tertiary amine, cocaine ![]() |
---|---|
Get use | Medication ![]() |
Conjugate acid | protonated cocaine ![]() |
Stereoisomer of | Methyl (1S,2R,3R,5R)-3-(benzoyloxy)-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate, pseudococaine, Pseudoallococaine, Methyl (1R,2R,3R,5S)-3-benzoyloxy-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate ![]() |
Chemical formula | C₁₇H₂₁NO₄ ![]() |
Canonical SMILES | CN1C2CCC1C(C(C2)OC(=O)C3=CC=CC=C3)C(=O)OC ![]() |
Isomeric SMILES | CN1[C@H]2CC[C@@H]1[C@H]([C@H](C2)OC(=O)C3=CC=CC=C3)C(=O)OC ![]() |
Safety classification and labelling | Regulation (EC) No. 1272/2008 ![]() |
Active ingredient in | Goprelto, crack ![]() |
Medical condition treated | pain, cough ![]() |
Physically dey interact plus | 5-hydroxytryptamine receptor 3A ![]() |
Route of administration | topical medication, insufflation ![]() |
Pregnancy category | US pregnancy category C ![]() |
Natural product of taxon | Erythroxylum coca, Erythroxylum novogranatense ![]() |
Cocaine (from French cocaïne, from Spanish coca, ultimately from Quechua kúka)[1] be a tropane alkaloid wey dey act as a central nervous system (CNS) stimulant.[2][3] Na dem traditionally use Coca by indigenous South Americans for various purposes for over a thousand years.[4] As an extract, cocaine be rarely buh formally used as a local anaesthetic anaa diagnostic tool by medical practitioners insyd sam countries. However, chaw cocaine use today be recreational drug use, wey be consumed illegally make e produce euphoria den act as an aphrodisiac.[5][6]
Dem primarily dey obtain Cocaine from de leaves of two coca species native to South America: Erythroxylum coca den E. novogranatense.[7][8] After extraction from de plant, den further processing into cocaine hydrochloride (powdered cocaine), de drug be administered by ebe either snorted, dem apply am topically to de mouth, anaa dissolved den injected into a vein. Dem sanso fi turn am into free base form (typically crack cocaine), insyd wich e fi be heated til sublimated den then de vapours fi be inhaled.[9]
Cocaine dey stimulate de mesolimbic pathway insyd de brain,[8] wey dey produce mental effects such as intense happiness, sexual arousal, loss of reality, den agitation, along plus physical effects like fast heart rate, sweating, den dilated pupils.[9] High doses fi lead to high blood pressure anaa elevated body temperature.[10] Effects typically dey begin within seconds to minutes den dey last five to ninety minutes dey depend on administration route.[9] Secof ein topical anesthetic den vasoconstrictor properties, e be occasionally used insyd surgeries wey dey involve de pharynx anaa nasopharynx make e reduce pain, bleeding, den vocal cord spasm.[11] Cocaine dey act as a serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI),[12][13] increasing levels of serotonin, norepinephrine, den dopamine insyd de synaptic cleft, wey dey lead to heightened post-synaptic activation, plus dopamine wey dey contribute to euphoria den arousal, den de oda monoamines wey dey enhance additional effects.[12][14][15][16] E dey cross de blood–brain barrier mainly via a proton-coupled organic cation antiporter[17][18] den, to a lesser extent, by passive diffusion.[19]
A single dose of cocaine dey induce tolerance to de drug ein effects.[20] Repeated use dey likely to result for addiction.[21] Addicts wey abstain from cocaine fi experience prolonged craving wey dey last for chaw months.[22][23] Abstaining addicts sanso experience modest drug withdrawal symptoms wey dey last up to 24 hours, plus sleep disruption, anxiety, irritability, fatigue, lethargy, depression, decreased libido, den decreased ability to feel pleasure.[8][24] Use of cocaine dey increase de overall risk of death, den intravenous use dey potentially increase de risk of trauma den infectious diseases such as blood infections den HIV thru needle sharing. E sanso dey increase risk of stroke, heart attack, cardiac arrhythmia, lung injury (wen e be smoked), den sudden cardiac death.[8][25] Illicitly cocaine dem dey sell fi be adulterated plus fentanyl, local anesthetics, levamisole, cornstarch, quinine, anaa sugar, wich fi result for additional toxicity.[26][27] Insyd 2017, na de Global Burden of Disease Study find say cocaine use cause around 7,300 deaths annually.[28]
References
[edit | edit source]- ↑ "Cocaine". American Heritage Dictionary. Archived from the original on 3 January 2023. Retrieved 3 January 2023.
- ↑ "Cocaine and crack drug profile | www.euda.europa.eu". www.euda.europa.eu.
- ↑ "Cocaine - Alcohol and Drug Foundation". adf.org.au (in English).
- ↑ Hesse M (2002). Alkaloids: Nature's Curse or Blessing?. Weinheim: Wiley-VCH. p. 304. ISBN 978-3-906390-24-6.
- ↑ "Cocaine & Crack". Erowid.
- ↑ "Cocaine". DEA (in English).
- ↑ Plowman T (June 1982). "The identification of coca (Erythroxylum species): 1860–1910". Botanical Journal of the Linnean Society. 84 (4): 329–353. doi:10.1111/j.1095-8339.1982.tb00368.x.
- ↑ 8.0 8.1 8.2 8.3 Pomara C, Cassano T, D'Errico S, Bello S, Romano AD, Riezzo I, Serviddio G (2012). "Data available on the extent of cocaine use and dependence: biochemistry, pharmacologic effects and global burden of disease of cocaine abusers". Current Medicinal Chemistry. 19 (33): 5647–57. doi:10.2174/092986712803988811. PMID 22856655.
- ↑ 9.0 9.1 9.2 Zimmerman JL (October 2012). "Cocaine intoxication". Critical Care Clinics. 28 (4): 517–26. doi:10.1016/j.ccc.2012.07.003. PMID 22998988.
- ↑ Connors NJ, Hoffman RS (November 2013). "Experimental treatments for cocaine toxicity: a difficult transition to the bedside". The Journal of Pharmacology and Experimental Therapeutics. 347 (2): 251–7. doi:10.1124/jpet.113.206383. PMID 23978563. S2CID 6767268.
- ↑ Hamdan AL, Sataloff RT, Hawkshaw MJ (2022). "Topical Anesthesia in Office-Based Laryngeal Surgery". Office-Based Laryngeal Surgery. USA: Springer. pp. 123–137. doi:10.1007/978-3-030-91936-8_6. ISBN 978-3-030-91935-1. Archived from the original on 18 July 2022. Retrieved 18 July 2022.
- ↑ 12.0 12.1 Azizi SA (December 2020). "Monoamines: Dopamine, Norepinephrine, and Serotonin, Beyond Modulation, "Switches" That Alter the State of Target Networks". The Neuroscientist. 28 (2): 121–143. doi:10.1177/1073858420974336. ISSN 1073-8584. PMID 33292070. S2CID 228080727.
- ↑ Cheng MH, Block E, Hu F, Cobanoglu MC, Sorkin A, Bahar I (2015). "Insights into the Modulation of Dopamine Transporter Function by Amphetamine, Orphenadrine, and Cocaine Binding". Frontiers in Neurology. 6: 134. doi:10.3389/fneur.2015.00134. PMC 4460958. PMID 26106364.
- ↑ Proebstl L, Kamp F, Manz K, Krause D, Adorjan K, Pogarell O, Koller G, Soyka M, Falkai P, Kambeitz J (June 2019). "Effects of stimulant drug use on the dopaminergic system: A systematic review and meta-analysis of in vivo neuroimaging studies". European Psychiatry. 59: 15–24. doi:10.1016/j.eurpsy.2019.03.003. PMID 30981746.
- ↑ "How does cocaine produce its effects?". Archived from the original on 18 January 2022. Retrieved 12 May 2021.
- ↑ Wise RA, Robble MA (January 2020). "Dopamine and Addiction". Annual Review of Psychology. 71 (1): 79–106. doi:10.1146/annurev-psych-010418-103337. PMID 31905114.
- ↑ Sachkova A, Doetsch DA, Jensen O, Brockmöller J, Ansari S (October 2021). "How do psychostimulants enter the human brain? Analysis of the role of the proton-organic cation antiporter". Biochemical Pharmacology. 192: 114751. doi:10.1016/j.bcp.2021.114751. PMID 34464621.
- ↑ Tega Y, Tabata H, Kurosawa T, Kitamura A, Itagaki F, Oshitari T, Deguchi Y (January 2021). "Structural Requirements for Uptake of Diphenhydramine Analogs into hCMEC/D3 Cells Via the Proton-Coupled Organic Cation Antiporter". Journal of Pharmaceutical Sciences. 110 (1): 397–403. doi:10.1016/j.xphs.2020.09.001. PMID 32898521.
- ↑ Chapy H, Smirnova M, André P, Schlatter J, Chiadmi F, Couraud PO, Scherrmann JM, Declèves X, Cisternino S (October 2014). "Carrier-mediated cocaine transport at the blood–brain barrier as a putative mechanism in addiction liability". The International Journal of Neuropsychopharmacology. 18 (1): pyu001. doi:10.1093/ijnp/pyu001. PMC 4368859. PMID 25539501.
- ↑ Ambre JJ, Belknap SM, Nelson J, Ruo TI, Shin SG, Atkinson AJ (July 1988). "Acute tolerance to cocaine in humans". Clinical Pharmacology and Therapeutics. 44 (1): 1–8. doi:10.1038/clpt.1988.104. PMID 3390996. S2CID 44253676.
- ↑ "Cocaine". National Institute on Drug Abuse (NIDA) (in English).
- ↑ Paludetto LS, Florence LL, Torales J, Ventriglio A, Castaldelli-Maia JM (29 March 2024). "Mapping the Neural Substrates of Cocaine Craving: A Systematic Review". Brain Sciences. 14 (4): 329. doi:10.3390/brainsci14040329. PMC 11048489. PMID 38671981.
- ↑ Wolf ME (June 2016). "Synaptic mechanisms underlying persistent cocaine craving". Nature Reviews. Neuroscience. 17 (6): 351–365. doi:10.1038/nrn.2016.39. PMC 5466704. PMID 27150400.
- ↑ Walsh SL, Stoops WW, Moody DE, Lin SN, Bigelow GE (August 2009). "Repeated dosing with oral cocaine in humans: assessment of direct effects, withdrawal, and pharmacokinetics". Experimental and Clinical Psychopharmacology. 17 (4): 205–216. doi:10.1037/a0016469. PMC 2811070. PMID 19653786.
- ↑ Sordo L, Indave BI, Barrio G, Degenhardt L, de la Fuente L, Bravo MJ (September 2014). "Cocaine use and risk of stroke: a systematic review". Drug and Alcohol Dependence. 142: 1–13. doi:10.1016/j.drugalcdep.2014.06.041. PMID 25066468.
- ↑ Goldstein RA, DesLauriers C, Burda AM (January 2009). "Cocaine: history, social implications, and toxicity--a review". Disease-a-Month. 55 (1): 6–38. doi:10.1016/j.disamonth.2008.10.002. PMID 19081448.
- ↑ "Fentanyl-Adulterated Cocaine: Strategies To Address The New Normal". 25 April 2019. Archived from the original on 17 December 2022. Retrieved 17 December 2022.
- ↑ Roth GA, Abate D, Abate KH, Abay SM, Abbafati C, Abbasi N, Abbastabar H, Abd-Allah F, Abdela J, Abdelalim A, Abdollahpour I, et al. (GBD 2017 Causes of Death Collaborators) (November 2018). "Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980–2017: a systematic analysis for the Global Burden of Disease Study 2017". Lancet. 392 (10159): 1736–1788. doi:10.1016/S0140-6736(18)32203-7. PMC 6227606. PMID 30496103.
Read further
[edit | edit source]- Feiling T (2009). The Candy Machine: How Cocaine Took Over the World. London: Penguin. ISBN 978-0-14-103446-1.
- Gootenberg P, ed. (1999). Cocaine: Global Histories. London: Routledge. ISBN 978-0-203-02646-5.
- Madge T (2001). White Mischief: A Cultural History of Cocaine. Edinburgh: Mainstream Publishing Company. ISBN 978-1-84018-405-1.
- Spillane JF, ed. (2000). Cocaine: From Medical Marvel to Modern Menace in the United States, 1884–1920. Baltimore and London: The Johns Hopkins University Press. ISBN 978-0-8018-6230-4.
External links
[edit | edit source]- Pages using the JsonConfig extension
- CS1 English-language sources (en)
- Pages using Sister project links with wikidata mismatch
- Pages using Sister project links with hidden wikidata
- Cocaine
- 1855 introductions
- 1855 insyd de German Confederation
- 1855 insyd science
- Adulteration
- Alkaloids dem find insyd Erythroxylum
- Anorectics
- Benzoate esters
- Carboxylate esters
- Cardiac stimulants
- Cocaine insyd de United States
- Counterculture of de 1980s
- CYP2D6 inhibitors
- Euphoriants
- German inventions
- Glycine receptor agonists
- Local anesthetics
- Methyl esters
- Neurotoxins
- Otologicals
- Powders
- Secondary metabolites
- Serotonin–norepinephrine–dopamine reuptake inhibitors
- Sigma agonists
- Stimulants
- Sympathomimetic amines
- Teratogens
- Tropane alkaloids dem find insyd Erythroxylum coca
- Vasoconstrictors
- Translated from MDWiki