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Review
. 2022 Jul 15;23(14):7800.
doi: 10.3390/ijms23147800.

Ketamine plus Alcohol: What We Know and What We Can Expect about This

Natalia Harumi Correa Kobayashi  1 , Sarah Viana Farias  1 , Diandra Araújo Luz  1 , Kissila Márvia Machado-Ferraro  1 , Brenda Costa da Conceição  1 , Cinthia Cristina Menezes da Silveira  1 , Luanna Melo Pereira Fernandes  1 , Sabrina de Carvalho Cartágenes  1 , Vânia Maria Moraes Ferreira  2 , Enéas Andrade Fontes-Júnior  1 , Cristiane do Socorro Ferraz Maia  1
Affiliations
Review

Ketamine plus Alcohol: What We Know and What We Can Expect about This

Natalia Harumi Correa Kobayashi et al. Int J Mol Sci. .

Abstract

Drug abuse has become a public health concern. The misuse of ketamine, a psychedelic substance, has increased worldwide. In addition, the co-abuse with alcohol is frequently identified among misusers. Considering that ketamine and alcohol share several pharmacological targets, we hypothesize that the consumption of both psychoactive substances may synergically intensify the toxicological consequences, both under the effect of drugs available in body systems and during withdrawal. The aim of this review is to examine the toxicological mechanisms related to ketamine plus ethanol co-abuse, as well the consequences on cardiorespiratory, digestive, urinary, and central nervous systems. Furthermore, we provide a comprehensive discussion about the probable sites of shared molecular mechanisms that may elicit additional hazardous effects. Finally, we highlight the gaps of knowledge in this area, which deserves further research.

Keywords: addiction; alcohol; cardiorespiratory system; central nervous system; digestive system; drug abuse; ketamine; renal system; toxicological effects.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic pharmacological targets with potential synergism between deleterious effects of ketamine (red markers) and ethanol (black markers), highlighting (A) the main clinical manifestations already described and effects related to (B) hepatic, (C) cardiac, (D) respiratory, and (E) urinary damage. (+) Activation, elevation, potentiation, or stimulation; (−) inhibition or reduction; (X) blocking; (✸) damage or disruption.
Figure 2
Figure 2
Principal pharmacological mechanisms and repercussions of ketamine (red markers) or ethanol (black markers) use during drugs bioavailability on (A) glutamatergic, GABAergic, (B) dopaminergic, serotoninergic, cholinergic, and opioidergic neurotransmission on the central nervous system. (+) Activation, elevation, potentiation, or stimulation; (−) inhibition or reduction; (X) blocking.
Figure 3
Figure 3
Principal repercussions of ketamine (red markers) or ethanol (black markers) withdrawal on (A) glutamatergic, GABAergic, (B) dopaminergic, and serotoninergic neurotransmission on the central nervous system. (✸) Damage or disruption.
See this image and copyright information in PMC

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