肢体缺血再灌注损伤时血管组织一氧化氮产生途径及其机制  

Pathway and Mechanism of Nitric Oxide Production in Vascular Tissue on Limb Ischemia Reperfusion Injury

作　　者：张连元[1,2] 董淑云[1,2] 张之玮[1,2] 姚兴海[1,2] 苏静怡[1,2] 唐朝枢[1,2] 

机构地区：[1]华北煤炭医学院病理生理教研室 [2]北京医科大学心血管基础所

出　　处：《中华创伤杂志》1998年第S1期31-33,共3页Chinese Journal of Trauma

摘　　要：目的探讨肢体缺血再灌注（Ｉ／Ｒ）损伤时，血管组织一氧化氮（ＮＯ）产生的途径和机制。方法采用Ｒｏｓｅｎｔｈａｌ方法复制大鼠肢体Ｉ／Ｒ损伤模型。实验动物分为对照组和Ｉ／Ｒ组。分别测定血浆中、主动脉孵育液中ＮＯ－２含量和主动脉组织中ｃＧＭＰ含量及一氧化氮合酶（ＮＯＳ）活性，观察主动脉组织３Ｈ－Ｌ－精氨酸（３Ｈ－Ｌ－Ａｒｇ）的含量。结果（１）Ｉ／Ｒ组大鼠血浆和主动脉条孵育液中ＮＯ－２明显增加，主动脉ｃＧＭＰ含量也增高；（２）Ｉ／Ｒ组大鼠血管总ＮＯＳ（ｔＮＯＳ）活性增高，其中主要是诱导型ＮＯＳ（ｉＮＯＳ）活性增加；（３）Ｉ／Ｒ时血管组织中３Ｈ－Ｌ－Ａｒｇ的含量增多。结论肢体Ｉ／Ｒ后，血管组织Ｌ－Ａｒｇ跨膜转运加强，ｉＮＯＳ活性增加，导致非内皮源性ＮＯ生成增多。Aim To study the pathway and mechanism of nitric oxide (NO) production after ischemia reperfusion injury. Methods The model rats with limb ischemia reperfusion (I/R) injury were made with Rosenthai's method. The animals were divided into the control (normal) group and I/R group. The NO - 2 content in the plasma and aorta incubation, the cGMP content, the nitric oxide synthase (NOS) activity, and 3 H L arginine content in the aortic tissue were determined. Results In the I/R group, the plasma NO - 2 content, the aortic tissue NO - 2 and cGMP content increased, the inducible NOS activity increased, and the 3 H L arginine content of aortic tissue increased, compared with that of the control group .Conclusion After limb ischemia reperfusion, the L arginine transport and inducible NOS activity is enhanced and the endothelium undependant NO production increases.

关 键 词：肢体 缺血再灌注损伤 L-精氨酸 一氧化氮 一氧化氮合酶 

分 类 号：R658[医药卫生—外科学]