Protective effects of morphine on acute myocardial ischemiaª²reperfusion injury in rat and its influence on apoptosis of cardiomyocytes

    ZHAO Jianª²Hong, CHENG Yanª²Bin, ZHANG Zhengª²Yi, Na Tao

    1Department of Anatomy, 2 Center of Emergency, Second Affiliated Hospital, Lanzhou Medical College, Lanzhou 730000, China

    ¡¾Abstract¡¿ AIM: To explore the protective effects and mechanism of morphine in acute myocardial ischemiaª² reperfusion (AMIR) injury in rats and its influence on apoptosis of cardiomyocytes. METHODS: Seventy SD rats were included in the study, among which, forty were divided randomly into 4 groups: group A (n=10, ischemiaª²reperfusion group), group B (n=10, morphine preconditioning group), group C (morphine and naloxnehydrochorid group), and group D (normal control group). Thirty SD rats were used to calculate myocardial infarct size, with 10 in each group (A, B and C). The rat model of AMIR was established by tying and untying the left anterior descending branch (LAD) of rat coronary. The animals were then sacrificed and hearts were harvested for the determination of myocardial infarct size by TTC. The expression of Bclª²2 protein was observed by immunohistochemical technique. Radioimmunoassay was used to detect tumor necrosis factor alpha (TNFª²¦Á) in serum and routine method was used to detect creatine kinase (CKª²MB)in serum. RESULTS: The myocardium infarct size was smaller in group B than that in group A [(21.8¡À4.5) vs (37.5¡À5.8), P<0.01]. The expression of Bclª²2 protein in group B (¬·) increased significantly as compared with that in group A (+). TNFª²¦Á and CKª²MB were significantly lower in group A than those in group B [(0.42¡À0.08) vs(0.86¡À0.11), P<0.01; (39374¡À7885) vs(58511¡À4950), P<0.05]. CONCLUSION: Morphine can protect myocardium from AMIR injury by inhibiting the apoptosis of cardiomyocytes induced by TNFª²¦Á and by upª²regulating protein expression of Bclª²2 gene. ......