TY - JOUR
T1 - Ketamine modulates calcium homeostasis in hypoxia-reoxygenated cardiomyocytes
AU - Roh, Jang Ho
AU - Chang, Woochul
AU - Lim, Soyeon
AU - Song, Heesang
AU - Song, Byeong Wook
AU - Kim, Hye Jung
AU - Cha, Min Ji
AU - Jang, Yangsoo
AU - Chung, Nam Sik
AU - Hong, Yong Woo
AU - Hwang, Ki Chul
PY - 2008/9
Y1 - 2008/9
N2 - 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 ischemiareperfusion 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-type Ca2+-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 cardiomyocytesunder 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.
AB - 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 ischemiareperfusion 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-type Ca2+-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 cardiomyocytesunder 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.
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M3 - Article
AN - SCOPUS:84884546515
SN - 1738-2696
VL - 5
SP - 512
EP - 520
JO - Tissue Engineering and Regenerative Medicine
JF - Tissue Engineering and Regenerative Medicine
IS - 3
ER -