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目的 观察卡托普利和阿司匹林相互作用对培养乳鼠心肌细胞损伤的影响及其机制。方法 建立培养乳鼠心肌细胞损伤模型 ,分别采用酶联法及Griess试剂法测定培养液中乳酸脱氢酶和一氧化氮活性 ,采用Fura 2负载荧光技术检测胞内游离钙水平。结果 与模型组相比 ,卡托普利和阿司匹林均显著减少培养介质中LDH水平 ,显著增加NO生成 ,但二者联用存在显著的相互作用 ,且表现为拮抗效应。卡托普利显著减少胞内游离钙浓度 ,而阿司匹林单用及合用卡托普利均明显增加胞内游离钙浓度。结论 卡托普利和阿司匹林联用时对培养乳鼠心肌细胞损伤存在显著的相互作用 ,其机制与其减少NO生成及增加胞内游离钙浓度有关
Objective To observe the effect of captopril and aspirin on cultured neonatal rat cardiomyocyte injury and its mechanism. Methods Myocardial cell injury model was established in neonatal rats. The activities of lactate dehydrogenase and nitric oxide in the culture medium were determined by enzyme-linked immunosorbent assay (ELISA) and Griess reagent method respectively. The intracellular free calcium level was detected by Fura 2 loading fluorescence assay. Results Compared with the model group, both captopril and aspirin significantly reduced the level of LDH in the culture medium and significantly increased the production of NO. However, there was a significant interaction between the two and their antagonistic effects. Captopril significantly reduced intracellular free calcium concentration, and aspirin alone and combined captopril significantly increased intracellular free calcium concentration. Conclusions Both captopril and aspirin exert a significant interaction on cardiomyocyte injury in cultured neonatal rats, and its mechanism is related to the reduction of NO production and intracellular free calcium concentration