摘要
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).
Aim: To study the role of nitric oxide(NO) in the alteration of the reactivity to the vasoconstrictor of the isolated pulmary artery (PA) rings. Methods: In the common bile duct ligation rats (histologically, cirrhosis was present) , we tested the responses of PA rings to cumulative concentrations of phenylephrine (PE) before and after using the inhibitor of NO synthase (L-NAME) . Results: An impaired contractility to PE was observed in vitro in PA Rings from cirrhotic rats (Rmax was 131.51±6.9% in cirrhotic rats verse 162.86±11.30% in controls; P< 0.05) .Pretreatmet with L-NAME significantly reversed the vasocontractile response of the rings from cirrhotic tats (Rmas was increased to 175.958± 12.3%, P<0.05). In the controls Rmax was increased to 190.42±13.9% (P>0.05). Conclusions: The increase of NO may contribute to the pulmonary artery hyporeactivity to the PE in the cirrhotic rats.
出处
《胃肠病学和肝病学杂志》
CAS
1998年第4期320-323,共4页
Chinese Journal of Gastroenterology and Hepatology
基金
湖北省科委重点科技研究项目
关键词
肝硬化
肺动脉
一氧化氮
cirrhosis pulmonary artery nitric oxide