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目的 观察卡托普利对培养的原代心肌细胞缺氧再灌注损伤时心肌酶活性的影响 .方法 用培养的 SD乳鼠原代心室肌细胞建立缺氧再灌注模型 ,观察培养液中的肌酸磷酸激酶 ( CPK) ,碱性磷酸酶 ( AL P) ,谷草转氨酶 ( AST)及乳酸脱氢酶 ( L DH ) ,血管紧张素转换酶 ( ACE)活性的变化以及卡托普利对上述指标的影响 .结果 心肌细胞内 CPK,AL P,AST及 L DH,ACE的释放量随缺氧及再灌注时间的延长逐渐升高 ,缺氧早期 CPK,AL P反映细胞损伤的程度较 AST,ACE敏感 ,0 .5 mg.L- 1卡托普利可减少心肌细胞缺氧再灌注损伤时心肌酶的漏出 .结论 卡托普利可减轻心肌细胞缺氧再灌注损伤 ,对心肌细胞具有直接保护作用
Objective To observe the effect of captopril on the activity of myocardial enzymes in primary cultured neonatal rat cardiomyocytes subjected to hypoxia-reperfusion injury.Methods Hypoxia-reperfusion model was established in cultured primary ventricular myocytes of neonatal SD rats, The changes of activities of acid phosphatase (CPK), alkaline phosphatase (ALP), aspartate aminotransferase (AST) and lactate dehydrogenase (L DH) and angiotensin converting enzyme (ACE) .Results The release of CPK, ALP, AST and L DH, ACE in cardiomyocytes gradually increased with the prolongation of hypoxia and reperfusion time. Compared with AST and ACE, Sensitive, 0.5 mg.L-1 captopril could reduce the myocardial enzyme leakage during hypoxia-reperfusion injury.Conclusion Captopril can reduce myocardial ischemia reperfusion injury, myocardial cells have a direct protection effect