Liping Zhang1, Ying Zhang2, Xiaofeng Yu3, Huali Xu4, Dayuan Sui5, Xuezhong Zhao6. 1. MD, Department of Cardiovascular Medicine, First Hospital, Jilin University, Changchun, Jilin, P.R. China. Acquisition, analysis and interpretation of data; manuscript writing. 2. Master, Pharmacology, College of Pharmacy, Jilin University, Changchun, Jilin, P.R. China. Acquisition of data. 3. MD, Pharmacology, College of Pharmacy, Jilin University, Changchun, Jilin, P.R. China. Acquisition of data, technical procedures, histopathological examinations. 4. MD, Pharmacology, College of Pharmacy, Jilin University, Changchun, Jilin, P.R. China. Analysis and interpretation of data. 5. MD, Pharmacology, College of Pharmacy, Jilin University, Changchun, Jilin, P.R. China. Conception and design of the study, manuscript writing. 6. MD, Department of Cardiovascular Medicine, First Hospital, Jilin University, Changchun, Jilin, P.R. China. Conception and design of the study, critical revision, final approval.
Abstract
PURPOSE: To investigate the effect of alprostadil on myocardial ischemia/reperfusion (I/R) in rats. METHODS: Rats were subjected to myocardial ischemia for 30 min followed by 24h reperfusion. Alprostadil (4 or 8 μg/kg) was intravenously administered at the time of reperfusion and myocardial infarct size, levels of troponin T, and the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were measured. Antioxidative parameters, nitric oxide (NO) content and phosphorylated endothelial nitric oxide synthase 3 (p-eNOS) expression in the left ventricles were also measured. Histopathological examinations of the left ventricles were also performed. RESULTS: Alprostadil treatment significantly reduced myocardial infarct size, serum troponin T levels, and CK-MB and LDH activity (P<0.05). Furthermore, treatment with alprostadil significantly decreased malondialdehyde (MDA) content (P<0.05) and markedly reduced myonecrosis, edema and infiltration of inflammatory cells. Superoxide dismutase and catalase activities (P<0.05), NO level (P<0.01) and p-eNOS (P<0.05) were significantly increased in rats treated with alprostadil compared with control rats. CONCLUSION: These results indicate that alprostadil protects against myocardial I/R injury and that these protective effects are achieved, at least in part, via the promotion of antioxidant activity and activation of eNOS.
PURPOSE: To investigate the effect of alprostadil on myocardial ischemia/reperfusion (I/R) in rats. METHODS:Rats were subjected to myocardial ischemia for 30 min followed by 24h reperfusion. Alprostadil (4 or 8 μg/kg) was intravenously administered at the time of reperfusion and myocardial infarct size, levels of troponin T, and the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were measured. Antioxidative parameters, nitric oxide (NO) content and phosphorylated endothelial nitric oxide synthase 3 (p-eNOS) expression in the left ventricles were also measured. Histopathological examinations of the left ventricles were also performed. RESULTS:Alprostadil treatment significantly reduced myocardial infarct size, serum troponin T levels, and CK-MB and LDH activity (P<0.05). Furthermore, treatment with alprostadil significantly decreased malondialdehyde (MDA) content (P<0.05) and markedly reduced myonecrosis, edema and infiltration of inflammatory cells. Superoxide dismutase and catalase activities (P<0.05), NO level (P<0.01) and p-eNOS (P<0.05) were significantly increased in rats treated with alprostadil compared with control rats. CONCLUSION: These results indicate that alprostadil protects against myocardial I/R injury and that these protective effects are achieved, at least in part, via the promotion of antioxidant activity and activation of eNOS.