Inhibition by ketamine and amphetamine analogs of the neurogenic nitrergic vasodilations in porcine basilar arteries

Chen, Mei‐Fang; Lai, Su-Yu; Kung, Po-Cheng; Lin, Yo-Cheng; Yang, Hui-I; Chen, Po‐Yi; Liu, Ingrid Y.; Lua, Ahai C.; Lee, Tony Jer‐Fu

doi:10.1016/j.taap.2016.05.020

Cited by 4 publications

(2 citation statements)

References 47 publications

(75 reference statements)

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“…His encephalography was associated with ketamine use, as he was a young man without a cerebral disease history. Ketamine has a direct negative inotropic effect and an indirect stimulatory effect due to activation of the sympathetic system by blocking nicotinic acetylcholine receptors located on cerebral perivascular sympathetic nerves, resulting in diminished neurogenic vasodilation and normal blood flow to the brainstem (55), which may explain the patient's encephalatrophy. The patient was anaemic, which was discovered after the brain atrophy, but the anaemia could not explain such severe encephalatrophy.…”

Section: Discussionmentioning

confidence: 99%

Severe Encephalatrophy and Related Disorders From Long-Term Ketamine Abuse: A Case Report and Literature Review

Lin-ying

Huang

Li³

et al. 2021

Front. Psychiatry

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Ketamine is a glutamate N-methyl D-aspartate receptor antagonist and an anaesthetic agent that has been effectively used to treat depression. However, ketamine has also been increasingly used for recreational purposes. The dissociative side-effects of ketamine use, such as hallucinations, are the reason for abuse. Additionally, long-term ketamine abuse has been highly associated with liver-gallbladder and urinary symptoms. The present study reports the case of a 28-year-old young male adult with an 8-year history of daily inhalation of ketamine. We investigated the association between ketamine abuse and the mechanism of its adverse effects, particularly encephalatrophy, and attempted to find a link between these disorders. These results would help us to better understand ketamine usage, ketamine abuse effects and the addictive mechanism. To the best of our knowledge, the present case is the first report of severe brain atrophy related to ketamine abuse. Details of the patient are presented and the mechanism of the encephalatropy-associated ketamine abuse is discussed. Furthermore, organ dysfunction following chronic ketamine abuse may indicate that the side effects are the result of comprehensive action on multiple regions in the brain.

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Section: Discussionmentioning

confidence: 99%

Severe Encephalatrophy and Related Disorders From Long-Term Ketamine Abuse: A Case Report and Literature Review

Lin-ying

Huang

Li³

et al. 2021

Front. Psychiatry

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“…Erectile dysfunction (ED) has been observed in male ketamine abusers [ 30 , 31 ] and in ketamine-treated animals [ 32 , 33 ]. Chen MF et al found that ketamine acutely blocked the nAChRs on cerebral perivascular sympathetic nerves, which then reduced nicotine-induced neurogenic vasodilation [ 34 , 35 ]. However, the acute effects of ketamine on penile erections are unknown.…”

Section: Introductionmentioning

confidence: 99%

The Acute Effects and Mechanism of Ketamine on Nicotine-Induced Neurogenic Relaxation of the Corpus Cavernosum in Mice

Chao

Lim

et al. 2023

IJMS

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The present study aimed to investigate the acute effects and the mechanism of ketamine on nicotine-induced relaxation of the corpus cavernosum (CC) in mice. This study measured the intra-cavernosal pressure (ICP) of male C57BL/6 mice and the CC muscle activities using an organ bath wire myograph. Various drugs were used to investigate the mechanism of ketamine on nicotine-induced relaxation. Direct ketamine injection into the major pelvic ganglion (MPG) inhibited MPG-induced increases in ICP. D-serine/L-glutamate-induced relaxation of the CC was inhibited by MK-801 (N-methyl-D-aspartate (NMDA) receptor inhibitor), and nicotine-induced relaxation was enhanced by D-serine/L-glutamate. NMDA had no effect on CC relaxation. Nicotine-induced relaxation of the CC was suppressed by mecamylamine (a non-selective nicotinic acetylcholine receptor antagonist), lidocaine, guanethidine (an adrenergic neuronal blocker), Nw-nitro-L-arginine (a non-selective nitric oxide synthase inhibitor), MK-801, and ketamine. This relaxation was almost completely inhibited in CC strips pretreated with 6-hydroxydopamine (a neurotoxic synthetic organic compound). Ketamine inhibited cavernosal nerve neurotransmission via direct action on the ganglion and impaired nicotine-induced CC relaxation. The relaxation of the CC was dependent on the interaction of the sympathetic and parasympathetic nerves, which may be mediated by the NMDA receptor.

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Differential blockade by huperzine A and donepezil of sympathetic nicotinic acetylcholine receptor-mediated nitrergic neurogenic dilations in porcine basilar arteries

Shih

Chen

et al. 2020

European Journal of Pharmacology

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Inhibition by ketamine and amphetamine analogs of the neurogenic nitrergic vasodilations in porcine basilar arteries

Cited by 4 publications

References 47 publications

Severe Encephalatrophy and Related Disorders From Long-Term Ketamine Abuse: A Case Report and Literature Review

Severe Encephalatrophy and Related Disorders From Long-Term Ketamine Abuse: A Case Report and Literature Review

The Acute Effects and Mechanism of Ketamine on Nicotine-Induced Neurogenic Relaxation of the Corpus Cavernosum in Mice

Differential blockade by huperzine A and donepezil of sympathetic nicotinic acetylcholine receptor-mediated nitrergic neurogenic dilations in porcine basilar arteries

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