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目的:探讨一氧化氮(NO)在肝硬化大鼠离体肺动脉对缩血管物质反应性改变中的作用.方法:采用胆总管结扎大鼠模型(组织学证实肝硬化存在,模型成功),检测给予NO合酶(NOS)抑制剂(L-NAME)前后离休肺动脉环对不同浓度苯肾上腺素(PE)的反应性.结果:肝硬化模型组大鼠离体肺动脉环对PE的收缩反应较对照组明显降低,最大收缩反应(R_(max))分别为131.51±6.95%,161.86%±11.30%,两组差异有显著意义(P<0.05).给予L-NAME预处理后,肝硬化模型组R_(max)上升至175.96±12.33%,与L-NAME处理前比较差异有显著意义(P<0.05);对照组上升至190.42±13.91%,差异无显著性(P>0.05).结论:肝硬化大鼠离体肺动脉对苯肾上腺素的反应性降低可能与NO合成增多有关
Objective: To investigate the role of nitric oxide (NO) in the reactivity of vasoconstrictors in isolated pulmonary arteries of cirrhotic rats.Methods: The model of common bile duct ligation in rats was established (histologically confirmed the presence of cirrhosis and the model was successful) The reactivity of pulmonary artery rings before and after the release of NO synthase (NOS) inhibitor (L-NAME) to different concentrations of phenylephrine (PE) was observed.Results: Compared with control (P <0.05). After pretreatment with L-NAME, the maximal contractile response (R max) were 131.51 ± 6.95% and 161.86% ± 11.30% R max increased to 175.96 ± 12.33%, which was significantly different from that before L-NAME treatment (P <0.05), while the control group increased to 190.42 ± 13.91%, with no significant difference (P> 0.05) .Conclusion: Reduced reactivity to phenylephrine in isolated rat pulmonary arteries may be related to increased NO synthesis