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目的：探讨血管紧张素转换酶抑制剂对缺氧心肌细胞的保护机制。方法：培养Ｗｉｓｔａｒ大鼠心肌细胞，７２小时后分为对照组、卡托普利组、依那普利拉组、缺氧组、缺氧加卡托普利组、缺氧加依那普利拉组。药物终浓度为１０－５ｍｏｌ／Ｌ。前３组采用有氧培养，后３组应用低糖无氧培养３０分钟。在ＭＰＶ３型显微分光光度计下测定心肌细胞内乳酸脱氢酶、琥珀酸脱氢酶相对含量，并取细胞上清液应用生化分析仪测定细胞内酶漏出情况。实验结果采用ｔ检验。结果：卡托普利和依那普利拉均可提高心肌细胞内乳酸脱氢酶含量（与对照组、缺氧组相比Ｐ＜０．０１）；减少缺氧心肌细胞内酶的漏出（与缺氧组相比Ｐ＜０．０１）。结论：血管紧张素转换酶抑制剂可明显改善缺氧心肌细胞糖代谢，加速糖酵解，减轻缺氧性损伤，对缺氧心肌细胞具有一定的保护作用。
Objective: To investigate the protective mechanism of angiotensin converting enzyme inhibitor on hypoxic cardiomyocytes. Methods: The myocardial cells of Wistar rats were cultured and divided into control group, captopril group, enalapril group, hypoxia group, hypoxia and captopril group, hypoxia and enalapril group Pull group. The final drug concentration is 10-5mol / L. The first three groups were aerobically cultured, and the latter three groups were cultured for 30 minutes under hypoxia and anaerobic conditions. The relative content of lactate dehydrogenase and succinate dehydrogenase in cardiomyocytes was measured under MPV3 spectrophotometer. The cell supernatant was assayed by biochemical analyzer for intracellular enzyme leakage. The experimental results using t test. Results: Both captopril and enalapril could increase lactate dehydrogenase in cardiomyocytes (P <0.01 compared with control group and hypoxia group), reduce enzyme leakage in hypoxic cardiomyocytes Hypoxic group compared with P <0.01). CONCLUSION: Angiotensin converting enzyme inhibitors can significantly improve glucose metabolism, accelerate glycolytic and hypoxic injury in hypoxic cardiomyocytes, and have a protective effect on hypoxic cardiomyocytes.