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采用离体兔胸主动脉淋浴灌注方法,探讨雷米普利拉(Ram)对氧自由基损伤血管内皮功能的保护作用及其机理.结果发现,电解Krebs液产生的氧自由基明显抑制血管内皮依赖性舒张,降低血管壁氧化氮(NO)和cGMP含量,并使丙二醛含量增加;Ram消除电解所致的上述作用,并呈现剂量依赖性;NO合成的前体物质─—L-精氨酸亦具有相似的保护作用;Ram和L-精氨酸的保护作用均可被NO合成酶抑制剂所阻断。这些结果提示,Ram抗氧自由基损伤血管内皮的作用可能与其促进内皮细胞合成,释放NO有关。P<0.01,comparedwithcontrol.P<0.05,P<0.01.comparedwithEle;P<0.01.comparedwithRamΔΔP<0.01.comparedwithL-Arg.SimilarresultwasobtainedinthetissuetreatedwithL-Arg.However.theeffectofRaniorLArgwasabrogatcdinthepresenceofNArg.Reductionbyelectrolysisofnitritevaluewasnotinfluenced?
To explore the protective effect and mechanism of Ramipril on endothelial dysfunction induced by oxygen free radicals in vitro using in vitro perfusion of rabbit aorta. The results showed that the oxygen free radicals produced by the electrolytic Krebs fluid significantly inhibited endothelium-dependent relaxation and decreased the contents of nitric oxide (NO) and cGMP in the blood vessel wall and increased the content of malondialdehyde. Ram eliminated the above effects caused by electrolysis and presented L-arginine, a precursor of NO, also has a similar protective effect; the protective effects of both Ram and L-arginine can be blocked by NO synthase inhibitors. These results suggest that Ram anti-oxidative damage of vascular endothelial role may be related to its promotion of endothelial cell synthesis, the release of NO. P <0.01, comparedwithcontrol. P <0.05, P <0.01. comparedwithEle; P <0.01. comparedwithRamΔΔP <0.01. comparedwithL-Arg. SimilarresultwasobtainedinthetissuetreatedwithL-Arg. However. theeffectofRaniorLArgwasabrogatcdinthepresenceofNArg. Reductionbyelectrolysisofnitritevaluewasnotinfluenced?