摘要
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 。
AIM To investigate the effects of captopril on the enzymatology of cultured anoxicreperfused ventricular myocardial cells. METHODS An anoxicreperfusion model was established by using cultured ventrical myocardial cells of neonate rats. The CPK, ALP, AST, LDH and ACE activity in medium of myocardial cells was measured for 60, 120 and 180 min after anoxia and 30 and 60 min after reperfusion and the effects of 0.5 mg·L -1 captopril on anoxicreperfused myocardial cells were studied. RESULTS The release of CPK, ALP, AST, LDH and ACE from the myocardial cells increased gradually as anoxia and reperfussion prolonged. In the early period of anoxia, the level of CPK and ALP was a more sensitive indicator of the extent of injury to the myocardial cells than that of AST and ACE. Meanwhile, 0.5 mg·L -1 captopril might reduce the leakage of enzymes significantly during anoxia and reperfussion. CONCLUSION That captopril might reduce the leakage of enzymes of cultured myocardial cells demonstrated that captopril might have a direct protective effect on myocardial cells afflicted with anoxicreperfusion injury.
出处
《第四军医大学学报》
2000年第5期627-629,共3页
Journal of the Fourth Military Medical University
