感染性休克下调大鼠血管内皮和血小板L-精氨酸／一氧化氮通路  

Septic shock down-regulates L-arginine /NOS/NO pathway of platelet and aortic intima in rats

作　　者：崔玉英[1] 唐朝枢[2] 耿彬[2] 冯浩楼[1] 

机构地区：[1]河北大学医学部东校区生理教研室,河北保定071000 [2]北京大学第一医院心血管研究所,北京100034

出　　处：《中国病理生理杂志》2008年第3期470-475,共6页Chinese Journal of Pathophysiology

基　　金：河北省科学技术研究与发展计划资助项目(No.06276121);保定市科技攻关课题资助项目(No.06F04);河北大学医学部科学研究基金项目(No.2007JY02)

摘　　要：目的:观察感染性休克对大鼠血小板及血管L-精氨酸(L-Arg)/一氧化氮合酶(NOS)/一氧化氮(NO)通路的影响及其相互联系,探讨感染性休克损伤的机制。方法:利用盲肠结扎并穿孔复制早期和晚期感染性休克大鼠模型,采用Greiss法测定血管各层及血小板孵育液亚硝酸盐(NO2-/NO3-)含量;以同位素示踪法检测其NOS活性及L-Arg转运。结果:早、晚期感染性休克大鼠血小板和主动脉内膜NO2-/NO3-水平、NOS活性及低亲合L-Arg转运量均显著低于假手术组(高亲合L-Arg转运量在早期休克增加、晚期休克降低);而中膜和外膜的NO2-/NO3-水平、NOS活性及L-Arg转运量则显著高于假手术组,均以休克晚期改变为显著。血小板和主动脉内膜NO2-/NO3-生成、NOS活性及高、低亲合L-Arg转运的改变均呈正相关(均P<0.01)。结论:感染性休克下调血管内膜和血小板的L-Arg/NO通路,上调血管中膜和外膜L-Arg/NO通路。提示检测血小板L-Arg/NO通路的变化可能反映休克时血管内皮功能的损伤。AIM ： To investigate alteration and cross link of the aortic and platelet endogenous L - arginine/ NOS/NO pathway induced by septic shock. METHODS： The septic shock model was made in rats by caecal ligation and puncture. NO2^-/NO3^- production released from aortic and platelet was measured with Greiss assay. NOS activity and L - arginine transport activity were detected by isotope tracer method. RESULTS： Both in early and late stage of septic shock, NO2^-/NO3^- production, NOS activity, and the L- arginine transport from the aorta intima and platelets were obviously decreased, while those of the aorta media and adventitia were obviously increased （ P 〈 0. 01 ） , but high - affinity L - arginine transport activity from the aorta intima and platelets was increased in early stage of septic shock （ P 〉 0. 05 and P 〈 0. 05）, as compared with the sham group, respectively. The inhibitory effects of NO2^-/NO3^-, NOS activity and the L - arginine transport showed a positive correlation between platelet and aortic intima （P 〈 0. 01 ）. CONCLUSION： Septic shock down -regulates endogenous L- arginine/NOS/NO pathway in aortic intima and platelet, up-regulates L- arginine/NOS/NO pathway of aortic media and adventitia. Detection of the alteration of endogenous L - arginine/NOS/NO pathway in platelet might act as an indirect method to assess the endothelial dysfunction involving the pathogensis of septic shock.

关 键 词：休克 脓毒性 血管内膜 血小板 一氧化氮 一氧化氮合酶 精氨酸 

分 类 号：R363.2[医药卫生—病理学] R631.4[医药卫生—基础医学]