内源性一氧化氮在肠系膜上动脉闭塞性休克中的保护作用  

Protected effect of Endogenous Nitric Oxide on Superior Mesenteric Artery Occlusion(SMAO) Shock

作　　者：凌毅群[1] 万梅[2] 刘彬 

机构地区：[1]河北医科大学第二医院普通外科,050000 [2]河北医科大学病理生理教研室 [3]河北医科大学第三医院泌尿外科

出　　处：《河北医药》1997年第2期65-66,共2页Hebei Medical Journal

摘　　要：实验采用兔肠系膜上动脉闭塞性(SMAO)休克模型,测定了休克前后血中一氧化氮(NO)的含量,动态观察了NO合成抑制剂L-NNA对休克时平均动脉血压(MAP)和肺动脉压(PAP)及对生存时间的影响,并测定了血中丙二醛(MDA)的含量。发现SMAO休克后血中NO含量与休克前相比无明显差异。注入L-NNA后显著增加了休克后PAP,缩短了存活时间,并使血中MDA含量明显增加。提示内源性NO对兔SMAO休克具重要的保护作用。The contents of NO in blood were determined in SMAO shock in rabbits. The effects of the inhibitor of NO, L-NNA on the mean artery pressure (MAP), pulmonary artery pressure(PAP)and survival time were also observed during the shock period. The results showed that the change of NO in blood was not significant before and after shock. PAP increased, survival time is shorttcr and MDA content increased after L-NNA infusion. It is suggested that endogenous NO has the very important protected ef-fect on SMAO shock in rabbits.

关 键 词：休克 肠系膜上动脉闭塞 内源性一氧化氮 SMAO 动物模型 

分 类 号：R657.2[医药卫生—外科学] R605.971[医药卫生—临床医学]