The Possible Mechanism of Cardioplegia-induced Cardiomyocytic Apoptosis After Global Cardiac Ischemia/Reperfusion Injury

• Main Authors: Yeh, Chi-Hsiao, 葉集孝
• Other Authors: Lin, Pyng Jing
• Format: Others
• Language: en_US
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/09562097493886012514

博士 === 長庚大學 === 臨床醫學研究所 === 92 === Hyperkalemic crystalloid cardioplegic solutions have been widely used for myocardial protection in cardiac surgery. However, they were only partially cardioprotective and ventricular dysfunction has been observed while inducing electromechanical arrest. Cardiomyocytic apoptosis might play an important role on the ischemia/reperfusion injury during cardioplegia-induced global cardiac arrest under cardiopulmonary bypass. In this research, we first identified that the differences of cardioprotective effect of various cardioplegic solutions came from the difference of the occurrence of cardiomyocytic apoptosis. Also, we found that the different cardioplegic solutions had different protective effects on the coronary endothelium, a major source of nitric oxide. From the results of the first part of this research, we utilized differential display polymerase chain reaction to identify the possible signal pathway of apoptosis during cardioplegia-induced cardiac arrest under cardiopulmonary bypass. Also, we determined that if nitric oxide had a role on the prevention of the occurrence of cardiomyocytic apoptosis. The inflammatory cytokines which were induced by cardiopulmonary bypass had been proved to be a major contributor of the postoperative myocardial dysfunction. Nuclear factor kappa B had a crucial role on the control of the inflammatory cascade. Using curcumin, an inhibitor of nuclear factor kappa B, we demonstrated that inhibition of the inflammatory signal transduction into the cardiomyocytes could diminish the cascade activation of the inflammatory cytokines, decrease the occurrence of apoptosis, and preserve the myocardial function.