Jump to content

Trip killer

Add links
From Wikipedia, the free encyclopedia

A trip killer, or hallucinogen antidote, is a drug that aborts or reduces the effects of a hallucinogenic drug experience (or 'trip').[1][2][3][4][5] As there are different types of hallucinogens that work in different ways, there are different types of trip killers.[6][7][8] They can completely block or reduce the effects of hallucinogens[6] or they can simply provide anxiety relief and sedation.[3] Examples of trip killers, in the case of serotonergic psychedelics, include serotonin receptor antagonists, like antipsychotics and certain antidepressants, and benzodiazepines.[4][6] Trip killers are sometimes used by recreational psychedelic users as a form of harm reduction to manage so-called bad trips, for instance difficult experiences with prominent anxiety.[2][4] They can also be used clinically to manage effects of hallucinogens, like anxiety and psychomotor agitation, for instance in the emergency department.[3][9]

Serotonergic psychedelic antidotes

[edit]
See also: Trazodone § Antagonism of serotonergic psychedelics

Serotonergic psychedelics, such as psilocybin (found in psilocybin mushrooms), lysergic acid diethylamide (LSD), mescaline (found in peyote cactii), and dimethyltryptamine (DMT) (found in ayahausca), are thought to produce their hallucinogenic effects via activation of the serotonin 5-HT2A receptor.[10][11][6] As a result, serotonin 5-HT2A receptor antagonists would theoretically be expected to block the hallucinogenic effects of serotonergic psychedelics.[6] Accordingly, the serotonin 5-HT2A receptor antagonists ketanserin, an antihypertensive agent, and risperidone, an antipsychotic, have been shown to block the effects of serotonergic psychedelics in clinical studies.[6][12][13][14] This includes the effects of psilocybin,[15][16][17] LSD,[18][19] mescaline,[20] and ayahausca.[21] Conversely, the antipsychotic chlorpromazine has shown inconsistent effects in reversing psychedelic effects,[6] while the antipsychotic haloperidol, which is a dopamine D2 receptor antagonist but not a serotonin 5-HT2A receptor antagonist, is ineffective.[6][22][15]

Cyproheptadine, a non-selective serotonin receptor antagonist (including of the serotonin 5-HT2A receptor), is used as an antidote in the treatment of serotonin syndrome (or serotonin toxicity) caused by serotonergic drugs, including the toxicity of serotonergic psychedelics like the NBOMe drugs.[23][24][25] Certain other serotonin receptor antagonists, like chlorpromazine, have also been used for such purposes.[25][26]

Recreational psychedelic users sometimes employ trip killers to abort psychedelic trips.[2][4][5] The most commonly encountered putative trip killers in a 2024 online study of Reddit social media postings were the benzodiazepines alprazolam and diazepam, the antipsychotic quetiapine, the antidepressant trazodone, and alcohol.[4][5][27] Others used less frequently included the benzodiazepines lorazepam, clonazepam, and etizolam, the antipsychotic olanzapine, and the antidepressant mirtazapine, among others.[4][5] Antipsychotics like quetiapine and olanzapine and antidepressants like trazodone and mirtazapine are all potent serotonin 5-HT2A receptor antagonists.[6][28][29] Conversely, benzodiazepines and alcohol act as positive allosteric modulators of the GABAA receptor and have anxiolytic and sedative effects.[30] Such effects can be useful in managing the effects of serotonergic psychedelics, including clinically in the case of benzodiazepines.[3][31] While employed by recreational users for harm-reduction purposes, the use of trip killers to abort the effects of psychedelics and other hallucinogens is not fully characterized and could pose medical risks.[1][4][5][27]

Other serotonin 5-HT2A receptor antagonists that may block or reduce the effects of serotonergic psychedelics include other antipsychotics, like pipamperone, other antidepressants, like mianserin, nefazodone, and etoperidone, and the antimigraine agent pizotifen, among others.[6] The selective serotonin 5-HT2A receptor antagonist pimavanserin is also being studied as a blocker of the effects of psychedelics.[32] Conversely, in spite of variably acting as serotonin 5-HT2A receptor antagonists, tricyclic antidepressants (TCAs), including desipramine, imipramine, and clomipramine, have paradoxically been reported to potentiate the effects of serotonergic psychedelics rather than diminish them.[6] Other drugs that have been reported to potentiate rather than inhibit the effects of serotonergic psychedelics include lithium, reserpine, pindolol, and methysergide.[6] Pindolol, a beta blocker and serotonin 5-HT1A receptor antagonist, has been reported to potentiate the hallucinogenic effects of DMT by 2- to 3-fold in humans.[33][34]

High-dose niacin (vitamin B3) was reported to reduce and block the effects of LSD in one early clinical study.[6][35][36] However, a subsequent clinical study attempting to replicate the findings found that it was not effective for this purpose.[35] Azacyclonol, a claimed ataractive (i.e., non-antipsychotic hallucination-suppressing medication) that is no longer marketed, likewise seems to be ineffective.[6]

Besides serotonin 5-HT2A receptor antagonists, other serotonergic drugs may also diminish the effects of serotonergic psychedelics.[6] Examples include serotonin 5-HT1A receptor agonists like buspirone, serotonin reuptake inhibitors like the selective serotonin reuptake inhibitors (SSRIs) (e.g., fluoxetine, paroxetine, sertraline) and serotonin–norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs) (e.g., phenelzine, nialamide, isocarboxazid).[6] Buspirone, a partial agonist of the serotonin 5-HT1A receptor, has specifically been found to markedly attenuate the visual and certain other effects of psilocybin, although it did not completely block the hallucinogenic effects of psilocybin.[6][37][33] The reduced effects of psychedelics in the case of concomitant drugs that elevate serotonin levels may be due to desensitization of serotonin 5-HT2A receptors.[6] Although MAOIs can diminish the effects of serotonergic psychedelics, it must be noted that some serotonergic psychedelics, such as DMT, are highly susceptible substrates for monoamine oxidase (MAO), and hence can simultaneously be greatly potentiated by MAOIs (as in ayahausca).[6][38]

Non-hallucinogenic partial agonists of the serotonin 5-HT2A receptor with sufficiently low intrinsic activity, such as 2-bromo-LSD and lisuride, are effective in blocking the hallucinogenic effects of serotonergic psychedelics as well.[39][40]

Other non-serotonergic drugs that may block or reduce the effects of serotonergic psychedelics based on animal studies include AMPA receptor antagonists, metabotropic glutamate mGlu2 and mGlu3 receptor agonists, μ-opioid receptor agonists, and adenosine A1 receptor agonists.[22][41][42]

Antidotes of other hallucinogens

[edit]

Cannabinoid CB1 receptor antagonists like rimonabant, drinabant, and surinabant have been found to block or reduce the psychoactive effects of cannabinoids in clinical studies and could be useful as antidotes against cannabinoid toxicity.[7][43] Likewise, the hallucinogenic and other effects of κ-opioid receptor agonists like salvinorin A (found in Salvia divinorum), butorphanol, and pentazocine have been shown to be blocked by the non-selective opioid receptor antagonist naltrexone in clinical studies.[8][44][45][46] Although clinical management of antimuscarinic deliriant intoxication and poisoning, for instance due to scopolamine, is usually supportive, acetylcholinesterase inhibitors, such as physostigmine, have sometimes been used in this context as well.[47][48] Benzodiazepines and antipsychotics have also been used in such situations.[47][48]

Although trip killers exist for certain types of hallucinogens, antidotes do not exist for all types of hallucinogens, for instance NMDA receptor antagonist dissociatives like ketamine and phencyclidine (PCP).[49][3][50] NMDA receptor agonists, which theoretically could reverse the effects of NMDA receptor antagonists, can produce excitotoxic neurotoxicity and convulsions, which limits their potential medical use.[51][52][53] In any case, benzodiazepines can be useful in managing dissociative intoxication.[9][49] As with NMDA receptor antagonists, there is no antidote for Amanita muscaria intoxication.[54][55]

References

[edit]
  1. ^ a b Muir OS, Shinozuka K, Beutler BD, Arenas A, Cherian K, Evans VD, Fasano C, Tabaac BJ (2024). "Psychedelic Therapy: A Primer for Primary Care Clinicians-The Strengths, Weaknesses, Opportunities, and Threats of Psychedelic Therapeutics". Am J Ther. 31 (2): e178–e182. doi:10.1097/MJT.0000000000001720. PMID 38518273. When psychedelics are used in recreational contexts without adequate supervision, they can lead to tragic outcomes.20 There are rare reports of serious adverse effects, including psychosis and even suicide, arising from recreational use.21 Methods for subduing socalled "bad trips" in recreational settings include potentially dangerous habits, such as taking benzodiazepines, which are known to be "trip killers."22
  2. ^ a b c Bellanavidanalage Gothami Ayanthie Vis Jayasinha (8 February 2024). Towards Safer Trips: Exploring Harm Reduction Strategies for Recreational Psychedelic Use in Aotearoa New Zealand (Thesis). University of Otago. Retrieved 3 October 2024. Another form of mixing substances involves the use of trip killers; a pharmacological coping strategy aimed to reduce the negative effects of a psychedelic experience by consuming a different substance (Suran, 2024). While this is a new concept and an under researched area, there are reports of trip killers being effective in reducing the negative effects of a psychedelic experience (Suran, 2024). One study gathered research from reddit, an online social media platform, investigating the usage of trip killers during challenging psychedelic experiences (Suran, 2024). The most popular and effective trip killers used were prescription medication, with 47% reporting the use of benzodiazepines as they reduce anxiety, followed by the use of antipsychotic and antidepressant medication (Suran, 2024). However, there are risks in mixing substances with psychedelic drugs, and subjectivity in the effectiveness. As some individuals may experience positive effects, while for others it may lead to negative effects (Suran, 2024). Therefore, it is recommended that before using trip killers, individuals should try other non- pharmacological coping strategies to reduce the negative effects of the psychedelic drug (Gable, 2004; Van Amsterdam et al., 2011). These factors discussed above, demonstrate the effectiveness of protective behaviours and harm reduction practices, in promoting safe psychedelic use and reducing harm.
  3. ^ a b c d e Leikin, Jerrold B.; Krantz, Anne J.; Zell-Kanter, Michele; Barkin, Robert L.; Hryhorczuk, Daniel O. (1989). "Clinical Features and Management of Intoxication Due to Hallucinogenic Drugs". Medical Toxicology and Adverse Drug Experience. 4 (5). Springer Science and Business Media LLC: 324–350. doi:10.1007/bf03259916. ISSN 0113-5244. PMID 2682130.
  4. ^ a b c d e f g Yates G, Melon E (January 2024). "Trip-killers: a concerning practice associated with psychedelic drug use". Emerg Med J. 41 (2): 112–113. doi:10.1136/emermed-2023-213377. PMID 38123961.
  5. ^ a b c d e Suran M (February 2024). "Study Finds Hundreds of Reddit Posts on "Trip-Killers" for Psychedelic Drugs". JAMA. 331 (8): 632–634. doi:10.1001/jama.2023.28257. PMID 38294772.
  6. ^ a b c d e f g h i j k l m n o p q r s Halman A, Kong G, Sarris J, Perkins D (January 2024). "Drug-drug interactions involving classic psychedelics: A systematic review". J Psychopharmacol. 38 (1): 3–18. doi:10.1177/02698811231211219. PMC 10851641. PMID 37982394.
  7. ^ a b Skolnick P, Crystal R (February 2020). "Cannabinoid1 (CB-1) receptor antagonists: a molecular approach to treating acute cannabinoid overdose". J Neural Transm (Vienna). 127 (2): 279–286. doi:10.1007/s00702-019-02132-7. PMC 7035232. PMID 31893308.
  8. ^ a b Clark SD, Abi-Dargham A (October 2019). "The Role of Dynorphin and the Kappa Opioid Receptor in the Symptomatology of Schizophrenia: A Review of the Evidence". Biol Psychiatry. 86 (7): 502–511. doi:10.1016/j.biopsych.2019.05.012. PMID 31376930. Finally, in a double-blind study of 24 healthy volunteers, Maqueda et al. (27) found that salvinorin A produced both visual and auditory changes that could be blocked by the kappa, mu, and delta receptor antagonist naltrexone (Table 2).
  9. ^ a b Bey T, Patel A (February 2007). "Phencyclidine intoxication and adverse effects: a clinical and pharmacological review of an illicit drug". Cal J Emerg Med. 8 (1): 9–14. PMC 2859735. PMID 20440387.
  10. ^ Nichols DE (April 2016). "Psychedelics". Pharmacol Rev. 68 (2): 264–355. doi:10.1124/pr.115.011478. PMC 4813425. PMID 26841800.
  11. ^ Nichols DE (2018). "Chemistry and Structure-Activity Relationships of Psychedelics". Curr Top Behav Neurosci. Current Topics in Behavioral Neurosciences. 36: 1–43. doi:10.1007/7854_2017_475. ISBN 978-3-662-55878-2. PMID 28401524.
  12. ^ Halberstadt, Adam L.; Nichols, David E. (2020). "Serotonin and serotonin receptors in hallucinogen action". Handbook of Behavioral Neuroscience. Vol. 31. Elsevier. pp. 843–863. doi:10.1016/b978-0-444-64125-0.00043-8. ISBN 978-0-444-64125-0. ISSN 1569-7339.
  13. ^ Canal CE (2018). "Serotonergic Psychedelics: Experimental Approaches for Assessing Mechanisms of Action". Handb Exp Pharmacol. Handbook of Experimental Pharmacology. 252: 227–260. doi:10.1007/164_2018_107. ISBN 978-3-030-10560-0. PMC 6136989. PMID 29532180. Reports from clinical trials conclude that the psychedelic effects of psilocybin and LSD are mediated by 5-HT2A receptors, because they are blocked by ketanserin (40 mg, P.O.), typically viewed as a selective 5-HT2A antagonist (Kometer et al. 2012; Kraehenmann et al. 2017; Preller et al. 2017; Quednow et al. 2012). Haloperidol, typically viewed as a selective dopamine D2 antagonist, is much less effective than ketanserin at blocking psilocybin's effects, but risperidone, an antipsychotic with combined D2/5-HT2 activity, is as effective as ketanserin (Vollenweider et al. 1998).
  14. ^ Holze F, Singh N, Liechti ME, D'Souza DC (May 2024). "Serotonergic Psychedelics: A Comparative Review of Efficacy, Safety, Pharmacokinetics, and Binding Profile". Biol Psychiatry Cogn Neurosci Neuroimaging. 9 (5): 472–489. doi:10.1016/j.bpsc.2024.01.007. PMID 38301886.
  15. ^ a b Vollenweider FX, Vollenweider-Scherpenhuyzen MF, Bäbler A, Vogel H, Hell D (December 1998). "Psilocybin induces schizophrenia-like psychosis in humans via a serotonin-2 agonist action". NeuroReport. 9 (17): 3897–3902. doi:10.1097/00001756-199812010-00024. PMID 9875725.
  16. ^ Carter OL, Hasler F, Pettigrew JD, Wallis GM, Liu GB, Vollenweider FX (December 2007). "Psilocybin links binocular rivalry switch rate to attention and subjective arousal levels in humans". Psychopharmacology (Berl). 195 (3): 415–424. doi:10.1007/s00213-007-0930-9. PMID 17874073.
  17. ^ Quednow BB, Kometer M, Geyer MA, Vollenweider FX (February 2012). "Psilocybin-induced deficits in automatic and controlled inhibition are attenuated by ketanserin in healthy human volunteers". Neuropsychopharmacology. 37 (3): 630–640. doi:10.1038/npp.2011.228. PMC 3260978. PMID 21956447.
  18. ^ Holze F, Vizeli P, Ley L, Müller F, Dolder P, Stocker M, Duthaler U, Varghese N, Eckert A, Borgwardt S, Liechti ME (February 2021). "Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects". Neuropsychopharmacology. 46 (3): 537–544. doi:10.1038/s41386-020-00883-6. PMC 8027607. PMID 33059356.
  19. ^ Becker AM, Klaiber A, Holze F, Istampoulouoglou I, Duthaler U, Varghese N, Eckert A, Liechti ME (February 2023). "Ketanserin Reverses the Acute Response to LSD in a Randomized, Double-Blind, Placebo-Controlled, Crossover Study in Healthy Participants". Int J Neuropsychopharmacol. 26 (2): 97–106. doi:10.1093/ijnp/pyac075. PMC 9926053. PMID 36342343.
  20. ^ Klaiber A, Schmid Y, Becker AM, Straumann I, Erne L, Jelusic A, Thomann J, Luethi D, Liechti ME (September 2024). "Acute dose-dependent effects of mescaline in a double-blind placebo-controlled study in healthy subjects". Transl Psychiatry. 14 (1): 395. doi:10.1038/s41398-024-03116-2. PMC 11442856. PMID 39349427.
  21. ^ Valle M, Maqueda AE, Rabella M, Rodríguez-Pujadas A, Antonijoan RM, Romero S, Alonso JF, Mañanas MÀ, Barker S, Friedlander P, Feilding A, Riba J (July 2016). "Inhibition of alpha oscillations through serotonin-2A receptor activation underlies the visual effects of ayahuasca in humans". Eur Neuropsychopharmacol. 26 (7): 1161–1175. doi:10.1016/j.euroneuro.2016.03.012. hdl:2117/101863. PMID 27039035.
  22. ^ a b Halberstadt AL (January 2015). "Recent advances in the neuropsychopharmacology of serotonergic hallucinogens". Behav Brain Res. 277: 99–120. doi:10.1016/j.bbr.2014.07.016. PMC 4642895. PMID 25036425.
  23. ^ Scotton WJ, Hill LJ, Williams AC, Barnes NM (2019). "Serotonin Syndrome: Pathophysiology, Clinical Features, Management, and Potential Future Directions". Int J Tryptophan Res. 12: 1178646919873925. doi:10.1177/1178646919873925. PMC 6734608. PMID 31523132.
  24. ^ Ordak M, Zmysłowska A, Bielski M, Rybak D, Tomaszewska M, Wyszomierska K, Kmiec A, Garlicka N, Zalewska M, Zalewski M, Nasierowski T, Muszynska E, Bujalska-Zadrozny M (2021). "Pharmacotherapy of Patients Taking New Psychoactive Substances: A Systematic Review and Analysis of Case Reports". Front Psychiatry. 12: 669921. doi:10.3389/fpsyt.2021.669921. PMC 8102790. PMID 33967865.
  25. ^ a b Jacobs, Elizabeth T; Akers, Katherine G; Vohra, Varun; King, Andrew M (10 October 2020). "Cyproheptadine for Serotonin Toxicity: an Updated Systematic Review and Grading of Evidence". Current Emergency and Hospital Medicine Reports. 8 (4). Springer Science and Business Media LLC: 151–159. doi:10.1007/s40138-020-00222-5. ISSN 2167-4884.
  26. ^ Chiew AL, Isbister GK (June 2024). "[Not Available]". Br J Clin Pharmacol (in French). doi:10.1111/bcp.16152. PMID 38926083.
  27. ^ a b Davidson, Colin (14 February 2024). "Using "trip killers" to cut short bad drug trips is potentially dangerous". The Conversation (UK Edition). SyndiGate Media Inc.: NA. Retrieved 3 October 2024.
  28. ^ Leysen JE (February 2004). "5-HT2 receptors". Curr Drug Targets CNS Neurol Disord. 3 (1): 11–26. doi:10.2174/1568007043482598. PMID 14965241.
  29. ^ Köhler S, Cierpinsky K, Kronenberg G, Adli M (January 2016). "The serotonergic system in the neurobiology of depression: Relevance for novel antidepressants". J Psychopharmacol. 30 (1): 13–22. doi:10.1177/0269881115609072. PMID 26464458.
  30. ^ Olsen RW (July 2018). "GABAA receptor: Positive and negative allosteric modulators". Neuropharmacology. 136 (Pt A): 10–22. doi:10.1016/j.neuropharm.2018.01.036. PMC 6027637. PMID 29407219.
  31. ^ Halpern, John H.; Suzuki, Joji; Huertas, Pedro E.; Passie, Torsten (2010). "Hallucinogens". Addiction Medicine. New York, NY: Springer New York. pp. 1083–1098. doi:10.1007/978-1-4419-0338-9_54. ISBN 978-1-4419-0337-2.
  32. ^ "Psilocybin Mechanism of Action (MOA)". ClinicalTrials.gov. Retrieved 13 November 2024.
  33. ^ a b Pokorny T, Preller KH, Kraehenmann R, Vollenweider FX (April 2016). "Modulatory effect of the 5-HT1A agonist buspirone and the mixed non-hallucinogenic 5-HT1A/2A agonist ergotamine on psilocybin-induced psychedelic experience". Eur Neuropsychopharmacol. 26 (4): 756–766. doi:10.1016/j.euroneuro.2016.01.005. PMID 26875114.
  34. ^ Strassman RJ (1996). "Human psychopharmacology of N,N-dimethyltryptamine". Behav Brain Res. 73 (1–2): 121–124. doi:10.1016/0166-4328(96)00081-2. PMID 8788488.
  35. ^ a b Murphree, Henry (1983). "The Pharmacology of Hallucinogens". Research Advances in Alcohol and Drug Problems. Boston, MA: Springer US. pp. 175–205. doi:10.1007/978-1-4613-3626-6_5. ISBN 978-1-4613-3628-0. In older work, various steroids (Bergen et al., 1960) including progesterone (Krus et al., 1961) were reported to be effective antagonists. This has not been replicated. In other early work, some compounds initially reported to be effective were not found to be so by other workers. These include azacyclonal (Fabing, 1955) and niacin (Agnew and Hoffer, 1955).
  36. ^ Agnew N, Hoffer A (January 1955). "Nicotinic acid modified lysergic acid diethylamide psychosis". J Ment Sci. 101 (422): 12–27. doi:10.1192/bjp.101.422.12. PMID 14368207.
  37. ^ Brandt SD, Kavanagh PV, Twamley B, Westphal F, Elliott SP, Wallach J, Stratford A, Klein LM, McCorvy JD, Nichols DE, Halberstadt AL (February 2018). "Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775)". Drug Test Anal. 10 (2): 310–322. doi:10.1002/dta.2222. PMC 6230476. PMID 28585392. Additionally, pretreatment with the 5‐HT1A agonist buspirone (20 mg p.o.) markedly attenuates the visual effects of psilocybin in human volunteers.59 Although buspirone failed to completely block the hallucinogenic effects of psilocybin, the limited inhibition is not necessarily surprising because buspirone is a low efficacy 5‐HT1A partial agonist.60 The level of 5‐HT1A activation produced by buspirone may not be sufficient to completely counteract the stimulation of 5‐HT2A receptors by psilocin (the active metabolite of psilocybin). Another consideration is that psilocin acts as a 5‐HT1A agonist.30 If 5‐HT1A activation by psilocin buffers its hallucinogenic effects similar to DMT58 then competition between psilocin and a weaker partial agonist such as buspirone would limit attenuation of the hallucinogenic response.
  38. ^ Egger, Klemens; Aicher, Helena D.; Cumming, Paul; Scheidegger, Milan (10 September 2024). "Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors". Cellular and Molecular Life Sciences. 81 (1). Springer Science and Business Media LLC. doi:10.1007/s00018-024-05353-6. ISSN 1420-682X. PMC 11387584.
  39. ^ Lewis V, Bonniwell EM, Lanham JK, Ghaffari A, Sheshbaradaran H, Cao AB, Calkins MM, Bautista-Carro MA, Arsenault E, Telfer A, Taghavi-Abkuh FF, Malcolm NJ, El Sayegh F, Abizaid A, Schmid Y, Morton K, Halberstadt AL, Aguilar-Valles A, McCorvy JD (March 2023). "A non-hallucinogenic LSD analog with therapeutic potential for mood disorders". Cell Rep. 42 (3): 112203. doi:10.1016/j.celrep.2023.112203. PMC 10112881. PMID 36884348.
  40. ^ Glatfelter GC, Pottie E, Partilla JS, Stove CP, Baumann MH (March 2024). "Comparative Pharmacological Effects of Lisuride and Lysergic Acid Diethylamide Revisited". ACS Pharmacol Transl Sci. 7 (3): 641–653. doi:10.1021/acsptsci.3c00192. PMID 38481684.
  41. ^ Marek GJ, Schoepp DD (2021). "Cortical influences of serotonin and glutamate on layer V pyramidal neurons". Prog Brain Res. 261: 341–378. doi:10.1016/bs.pbr.2020.11.002. PMID 33785135.
  42. ^ Marek GJ (August 2003). "Behavioral evidence for mu-opioid and 5-HT2A receptor interactions". Eur J Pharmacol. 474 (1): 77–83. doi:10.1016/s0014-2999(03)01971-x. PMID 12909198.
  43. ^ Bosquez-Berger, Taryn; Szanda, Gergő; Straiker, Alex (30 August 2023). "Requiem for Rimonabant: Therapeutic Potential for Cannabinoid CB1 Receptor Antagonists after the Fall". Drugs and Drug Candidates. 2 (3): 689–707. doi:10.3390/ddc2030035. ISSN 2813-2998.
  44. ^ Maqueda AE, Valle M, Addy PH, Antonijoan RM, Puntes M, Coimbra J, Ballester MR, Garrido M, González M, Claramunt J, Barker S, Lomnicka I, Waguespack M, Johnson MW, Griffiths RR, Riba J (July 2016). "Naltrexone but Not Ketanserin Antagonizes the Subjective, Cardiovascular, and Neuroendocrine Effects of Salvinorin-A in Humans". Int J Neuropsychopharmacol. 19 (7): pyw016. doi:10.1093/ijnp/pyw016. PMC 4966277. PMID 26874330.
  45. ^ Walsh SL, Chausmer AE, Strain EC, Bigelow GE (January 2008). "Evaluation of the mu and kappa opioid actions of butorphanol in humans through differential naltrexone blockade". Psychopharmacology (Berl). 196 (1): 143–155. doi:10.1007/s00213-007-0948-z. PMC 2766188. PMID 17909753.
  46. ^ Preston KL, Bigelow GE (February 1993). "Differential naltrexone antagonism of hydromorphone and pentazocine effects in human volunteers". J Pharmacol Exp Ther. 264 (2): 813–823. PMID 7679737.
  47. ^ a b Shim KH, Kang MJ, Sharma N, An SS (September 2022). "Beauty of the beast: anticholinergic tropane alkaloids in therapeutics". Nat Prod Bioprospect. 12 (1): 33. doi:10.1007/s13659-022-00357-w. PMC 9478010. PMID 36109439. The treatment of TA poisoning including gastric emptying, use of activated charcoal (0.5 to 1 g/kg in children or 25 to 100 g in adults) to absorb the drug and benzodiazepines for managing agitation [157, 158]. Physostigmine (an AChE inhibitor) is recommended in the case when both PNS and CNS are afected by anticholinergic poisoning [159, 160]. In such cases, intravenous dose of physostigmine (0.02 mg/kg for children and 0.5 to 2 mg/ kg for adults) is recommended [159]. Physostigmine is helpful in restoring the level of consciousness to its baseline [157] which is diferent from sedative action of benzodiazepines.
  48. ^ a b Bulut NS, Arpacıoğlu ZB (September 2022). "Acute onset psychosis with complex neurobehavioural symptomatology following the intramuscular injection of hyoscine butylbromide: a case report with an overview of the literature". Eur J Hosp Pharm. 29 (5): 294–297. doi:10.1136/ejhpharm-2020-002583. PMC 9660700. PMID 33376193. The most crucial intervention in the treatment of anticholinergic intoxication is without doubt the discontinuation of the suspected agent. Hospitalisation may be necessary for the close monitoring of severe cases. While physostigmine is commonly used as a specific antidote for anticholinergic toxicity, benzodiazepines and antipsychotics can prove to be useful in managing agitation, hallucinations, and agressive and self-mutilative behaviours as in our case.2
  49. ^ a b Schep LJ, Slaughter RJ, Watts M, Mackenzie E, Gee P (June 2023). "The clinical toxicology of ketamine". Clin Toxicol (Phila). 61 (6): 415–428. doi:10.1080/15563650.2023.2212125. PMID 37267048.
  50. ^ Jenkins, Amanda J.; Gates, Madeleine J. (2020). "Hallucinogens and Psychedelics". Principles of Forensic Toxicology. Cham: Springer International Publishing. pp. 467–489. doi:10.1007/978-3-030-42917-1_26. ISBN 978-3-030-42916-4.
  51. ^ Gonda X (2012). "Basic pharmacology of NMDA receptors". Curr Pharm Des. 18 (12): 1558–1567. doi:10.2174/138161212799958521. PMID 22280436.
  52. ^ Rana V, Ghosh S, Bhatt A, Bisht D, Joshi G, Purohit P (2024). "N-Methyl-D-Aspartate (NMDA) Receptor Antagonists and their Pharmacological Implication: A Medicinal Chemistry-oriented Perspective Outline". Curr Med Chem. 31 (29): 4725–4744. doi:10.2174/0109298673288031240405061759. PMID 38638036.
  53. ^ Rothman, Steven M.; Olney, John W. (1987). "Excitotoxity and the NMDA receptor". Trends in Neurosciences. 10 (7). Elsevier BV: 299–302. doi:10.1016/0166-2236(87)90177-9. ISSN 0166-2236.
  54. ^ Mitchel DH (1980). "Amanita mushroom poisoning". Annu Rev Med. 31: 51–57. doi:10.1146/annurev.me.31.020180.000411. PMID 6772091.
  55. ^ Rampolli FI, Kamler P, Carnevale Carlino C, Bedussi F (2021). "The Deceptive Mushroom: Accidental Amanita muscaria Poisoning". Eur J Case Rep Intern Med. 8 (3): 002212. doi:10.12890/2021_002212. PMC 7977045. PMID 33768066.
Retrieved from "https://wiki.riteme.site/w/index.php?title=Trip_killer&oldid=1259642875"