Ketamine modulates calcium homeostasis in hypoxia-reoxygenated cardiomyocytes.

Abstract

Ketamine is clinically used as an inducer of anesthesia in critically ill patients because it has more stable hemodynamics than barbiturates or inhaled anesthetic agent. It has been known the effect of anesthetic related with calcium homeostasis in myocardium but there are few studies for myocardial protection of ketamine from ischemia-reperfusion injury. We therefore observed protective effects of ketamine on survival of ischemia-reoxygenated cardiomyocytes in phosphorylation levels of Erk and Akt as well as suppression of pro-apoptotic protens, Bax and cytochrome C, and induction of anti-apoptotic protein, Bcl-2. Ketamine also overcame intracellular Ca2+, overload. We observed significant induction in transcript level of calreticulin, PMCA1, ion channels(L-typeCa(2+)-channel, Kir3.4, Kir6.1) and suppression in transcript level of calmodulin, and SERCA 2a in ketamine-treated cardiomyocytes. In conclusion, ketamine was protective of cardiomyocytes under hypoxia-reperfusion condition. Therefore, we have provided new insight into myocardial protection of anesthetic agents so a better understanding of the role of anesthetics in the prevention of myocardial injury may provide strategies to improve outcome.