Ketamine in insulin resistance: Pharmacokinetics, cardiovascular implications and cellular effects on cardiomyocytes.

Ketamine, a dissociative anaesthetic used for pain and depression, disrupts excitatory neurotransmission by blocking N-methyl-d-aspartate receptors and interacting with opioid and serotonin pathways. In patients with insulin resistance, ketamine's effects on glucose metabolism, mitochondrial function, and oxidative stress are worsened. This paper examines ketamine's pharmacokinetics, cardiovascular impact, and cellular effects on heart muscle cells, especially in insulin-resistant individuals. The findings highlight the need for careful administration and monitoring in these patients to balance therapeutic benefits against risks in those with metabolic or cardiovascular conditions.

Study at a glance

Abstract

Ketamine, a dissociative anaesthetic, has expanded its clinical use beyond anaesthesia to pain management and treatment-resistant depression. As an N-methyl-d-aspartate receptor antagonist, ketamine disrupts the excitatory neurotransmission via interaction with the opioid, alpha-amino-3-hydroxy-5-methyl-4-isooxazole-propionic acid receptor and serotonin pathways, contributing to its broad therapeutic potential. However, its use is not without risks. In patients with insulin resistance, ketamine's effect on glucose metabolism, mitochondrial function and oxidative stress are exacerbated. This paper explores ketamine's pharmacokinetics, cardiovascular impact and its cellular effects on cardiomyocytes, particularly in insulin-resistant individuals. The findings discussed emphasize the importance of careful administration and monitoring in these vulnerable populations to balance ketamine's therapeutic benefits against its potential risks in patients with underlying metabolic or cardiovascular conditions.