苯那普利对缺氧复氧心肌心胞内钙离子的影响及机制研究

The effects and mechanism of Benazepril on calcium in hypoxia-reoxygenation cardiomyocytes

目的研究苯那普利对乳鼠缺氧复氧心肌细胞内钙离子浓度的影响及作用机制。方法采用纯化培养的乳鼠心肌细胞复制缺血再灌注模型。实验分为4组，每组8例：空白对照组、单纯缺氧复氧组（H／R）、缺氧复氧＋苯那普利（1×10^6mol／L）组、缺氧复氧＋苯那普利（1×10^6mol／L）＋缓激肽B2受体拮抗剂（HOE140）（1×10^6mol／L）组。细胞缺氧1h，复氧2h后取细胞培养液测定乳酸脱氢酶（LDH），取细胞测定超氧化物歧化酶（SOD）的活性和丙二醛（MDA）含量，测定细胞内钙浓度。结果单纯缺氧复氧组与对照组比较，LDH、MDA、[Ca^2＋]i含量升高，SOD活性下降（P〈0．01）；苯那普利组与缺氧复氧组比较，LDH、MDA、[Ca^2＋]i含量降低，SOD活性升高（P〈0．01）；苯那普利＋HOE140组与苯那普利组比较，LDH、MDA、[Ca^2＋]i含量升高，SOD活性下降（P〈0．01）。结论苯那普利能降低细胞内钙离子浓度，有明显保护心肌的作用。其作用可能与激活激肽-缓激肽释放系统、抑制缓激肽的降解有关。

Objective To examine the effects of Benazepril on myocardial ischemia and reoxygenation injury and on calcium concentration in cardiomyocytes. Methods Cardiomyocytes were made into hypoxia-reoxygenation models. Tests were decided 4 groups： control group, hepoxia-reoxygenation group（ H/R ）,HR＋benapril（ 1×10^6 mol/L） group,H/R＋benazepril（1×10^6 mol/L）＋HOE140 （1×10^6 mol/L）. Samples were observed at the time of 1 h after hypoxia and 2 h after reoxygenation. Content of LDH, calcium concentration, malonialdehvde （MDA） level, super-oxide dismutes （SOD） activity were measured in cell cultured supernatant. Results Compare with control group, content of LDH, calcium concentration and MDA level increased, SOD activity decreased in H/R group, but SOD activity, content of LDH, MDA level,and calcium concentration decreased in henazepril group （P〈0.01）. In combined benazepril with hoel40 group, all index were reversed compare with benazpril group （1×10^6 mol/L）（P〈0.01 ）.Conclusion Benazepril can attenuate the overloading of intraeellular calcium, active kinin- bradykinin system, and inhibite bradykinin degradation.