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观察血管紧张素Ⅱ预处理（ＡｎｇⅡ）对乳鼠心肌细胞缺氧复氧（Ａ／Ｒ）损伤的影响，并探讨其作用机理。采用心肌细胞Ａ／Ｒ损伤模型，用血管紧张素Ⅱ进行预处理（ＡⅡＰＣ）。ＡⅡＰＣ能提高Ａ／Ｒ损伤后心肌细胞存活率（７６±３％比５２±２％，Ｐ＜０．０１，减少细胞ＭＤＡ产生（０．９５±０．０６比１．７２±０．０７ｎｍｏｌ／ｍｇｐｒ，Ｐ＜０．０１），减少乳酸脱氢酶漏出（３６．５±７．１比５６．３±９．３Ｕ／Ｌ，Ｐ＜０．０１），及蛋白漏出（０．３３±０．０４比０．４３±０．０７ｇ／Ｌ，Ｐ＜０．０１）。蛋白激酶Ｃ（ＰＫＣ）抑制剂Ｈ７完全阻断ＡⅡＰＣ的上述保护作用。结果提示ＡⅡＰＣ对乳鼠心肌细胞具有预处理保护作用，其机理是通过ＰＫＣ介导的。
To observe the effect of angiotensin Ⅱ preconditioning (AngⅡ) on neonatal rat cardiomyocyte hypoxia-reoxygenation (A / R) injury and its mechanism of action. Cardiomyocytes A / R injury model was used, with angiotensin Ⅱ pretreatment (A Ⅱ PC). AⅡPC increased myocardial cell viability after A / R injury (76 ± 3% vs. 52 ± 2%, P <0.01, decreased MDA production (0.95 ± 0.06 vs. 1.72 ± 0.07 nmol / mgpr, P <0.01), decreased lactate dehydrogenase leakage (36.5 ± 7.1 vs 56.3 ± 9.3 U / L, P <0.01) .04 vs 0.43 ± 0.07g / L, P <0.01) .Protein kinase C (PKC) inhibitor H7 completely blocked the above-mentioned protective effect of AⅡPC.The results suggest that AⅡPC pretreatment protected neonatal rat cardiomyocytes Its mechanism is mediated through PKC.