Mechanisms of Impaired Glucose Tolerance and Insulin Secretion during Isoflurane Anesthesia

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Abstract
DIABETES and hyperglycemia are significant predictors of perioperative cardiovascular morbidity and mortality.1 Several studies1–4 have shown that there is a strong correlation between blood glucose concentration and outcome in patients with coronary artery disease. These studies have suggested that a decrease in blood glucose concentration results in a lower rate of cardiovascular morbidity and mortality. Volatile anesthetics have been shown to have cardioprotective5,6 and vasodilative7–9 effects, which are mediated by activation of adenosine triphosphate–sensitive potassium (KATP) channels in cardiac myocytes and vascular smooth muscle cells, respectively. Volatile anesthetics have been known since the 1970s to impair insulin secretion and glucose utilization.10–15 However, the precise mechanism of action responsible for impaired insulin secretion in response to volatile anesthetics remains unclear.

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