内源性一氧化氮对大鼠慢性缺氧性肺动脉高压的调节作用  

The modulatory role of endogenous nitric oxide in the development of chronically hypoxic pulmonary hypertension in rats

作　　者：杜军保[1,2] 李万镇[1,2] 赵斌[1,2] 黎文[1,2] 

机构地区：[1]北京医科大学第一医院儿科 [2]北京积水谭医院

出　　处：《中华儿科杂志》1998年第2期89-91,共3页Chinese Journal of Pediatrics

基　　金：国家自然科学基金;卫生部全国优秀青年科技人才专项基金

摘　　要：目的探讨一氧化氮对慢性缺氧性肺动脉高压的调节作用。方法采用Ｗｉｓｔａｒ大鼠１８只，随机将各配伍组大鼠分别分配到组Ⅰ（对照组）、组Ⅱ（缺氧组）及组Ⅲ［缺氧加一氧化氮合酶抑制剂Ｎω－硝基－Ｌ－精氨酸甲酯（Ｌ－ＮＡＭＥ组）］。研究Ｌ－ＮＡＭＥ对缺氧性肺动脉高压的影响。结果与对照组相比，缺氧加Ｌ－ＮＡＭＥ注射的大鼠肺动脉平均压上升百分数（５８％±１２％）明显高于单纯缺氧大鼠（３４％±１５％）（ｔ＝３．０１３，Ｐ＜０．０１）；缺氧加Ｌ－ＮＡＭＥ注射大鼠血浆一氧化氮下降百分数（３８％±４％）明显大于单纯缺氧大鼠（１２％±１２％）（ｔ＝２７；０．０５＞Ｐ＞０．０２）。结论大鼠慢性缺氧时一氧化氮释放减少。Objective The aim of this study was to examine the modulatory role of endogenous nitric oxide in the development of chronically hypoxic pulmonary hypertension.Methods Eighteen Wistar rats were randomly divided into the following groups: group Ⅰ(control group), group Ⅱ (hypoxia group) and group Ⅲ [hypoxia+ N ω nitro L arginine methyl ester (L NAME) group]. The impacts of L NAME on hypoxic pulmonary hypertension were studied. Results The percentage of increase in pulmonary artery mean pressure as well as the percentage of decrease in plasma level of nitric oxide was more obvious in hypoxic pulmonary hypertensive rats with L NAME treatment than those without L NAME treatment (58±12%, 34±15%; 38±4%, 12±12%, all P < 0.05). Conclusion Nitric oxide release decreased during chronic hypoxia, which was probably involved in the mechanism of hypoxic pulmonary hypertension.

关 键 词：一氧化氮 低氧 高血压 肺性 

分 类 号：R543.203[医药卫生—心血管疾病]