败血症休克大鼠血管外膜L-精氨酸/一氧化氮合酶/一氧化氮通路的变化  

Changes of L-arginine,NOS/NO pathway in adventitia of rats with sepsis

作　　者：贾月霞[1] 潘舂水 杨靖辉[2] 耿彬[2] 张靓[2] 赵晶[2] 唐朝枢[2] 齐永芬[2] 

机构地区：[1]宁夏医学院病理生理教研室,宁夏银川750004 [2]北京大学医学部生理与病理生理学系,北京100083

出　　处：《中国病理生理杂志》2007年第3期417-422,共6页Chinese Journal of Pathophysiology

基　　金：国家重大基础发展规划资助项目(973)(NoG2000056905);国家自然科学基金资助项目(No30470693);中华人民共和国教育部重点基金资助项目(No105001);宁夏自然科学基金资助项目(NoN20542);宁夏科技攻关计划项目(2006)

摘　　要：目的:观察败血症休克大鼠主动脉外膜L-精氨酸(L-Arg)转运,一氧化氮合酶(NOS)活性和一氧化氮(NO)生成的变化。方法:雄性Wistar大鼠盲肠结扎并穿孔复制败血症休克模型。测定大鼠主动脉外膜亚硝酸盐(NOx)含量、一氧化氮合酶(NOS)活性及L-精氨酸(L-Arg)转运;RT-PCR方法测定诱导型一氧化氮合酶(iNOS)mRNA水平。结果:严重感染休克大鼠呈现严重的血流动力学紊乱,心功能抑制。败血症休克大鼠表现为严重的低血糖和高乳酸血症。血管外膜iNOS的mRNA水平均明显高于假手术组(均P<0.01),主动脉外膜NOx生成、NOS活性及L-Arg转运速率显著高于假手术组(P<0.01)。结论:败血症休克时血管外膜L-Arg/NOS/NO系统激活在败血症休克发病中可能起重要作用。AIM： In this study, we aimed to explore the alteration and pathophysiological significance of the L -arginine （L- Arg）/NOS/NO pathway in the adventitia of rats with sepsis. METHODS： Sepsis was induced by cecal ligation and puncture （CLP）. Rat cardiac function was determined. NO generation, NOS activity and L - Arg transport were measured. The iNOS mRNA levels was determined by using RT - PCR. RESULTS： Cecal ligation and puncture induced severe sepsis with severe low glucose, high lacticemia and cardiac function inhibition. The iNOS activity was increased by 2.8 - fold compared with controls （ P 〈 0. 01 ） and the iNOS mRNA level was elevated - 6 - fold （ P 〈 0. 01 ）. The NO level in plasma and incubation media （ incubation for 40 min） in the sepsis group was increased by 144% and 273% （both P 〈 0. 01 ）, respectively. CONCLUSION： The results demonstrated that the L- Arg, NOS/NO pathway was activated in vascular adventitia of rats with sepsis shock. The aortic adventitia L - Arg/NOS/NO pathway might play an important role in the pathogenesis of sepsis and septic shock.

关 键 词：休克 脓毒性 精氨酸 一氧化氮合酶 一氧化氮 

分 类 号：R363[医药卫生—病理学]