Abstract
The aim of this study is to investigate the mechanism of cardioprotective effects of diazoxide, a selective opener of mitochondrial ATP‐sensitive potassium channel (mitoKATP) in preserved heart. The isolated rat heart Langendorff model was used. The hearts were stored in 4°C Celsior solution in the presence or absence of diazoxide for 3, 6 or 9 h followed by 60 min of reperfusion. Apoptotic cardiomyocytes were detected by terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling (TUNEL) method. The expression of heat shock protein 70 (HSP 70) was also evaluated by western blotting analysis. The results showed that the percentage of apoptotic cells increased in a time‐dependent manner after hypothermic preservation. When compared with the 9 h control group, diazoxide (15, 30 or 45 μmol/L) reduced the percentage of apoptotic cells and increased the expression of HSP 70 protein in rat hearts suffered from 9 h of hypothermic preservation in a dosedependent manner. These results indicate that diazoxide could alleviate rat myocardial injury induced by ischemia‐ reperfusion through upregulation of HSP 70 protein expression.(This work was supported by the National Natural Science Foundation of China (No.30470635))
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