摘要
目的 采用大鼠内毒素血症模型 ,观察血浆、肝组织内皮素 - 1(ET - 1)和一氧化氮(NO)浓度的动态变化 ,探讨两者的相互关系。 方法 选用Wistar大鼠 15 0只 ,分为对照组、内毒素组、内毒素 +硝基左旋精氨酸组、内毒素 +左旋精氨酸组、内毒素 +内皮素抗体组 (每组 30只 )。观察伤后 3,6 ,9,12 ,2 4h血浆和肝组织ET - 1、NO浓度的变化。 结果 给予内毒素后 3h血浆、肝组织ET - 1和浓度均较对照组升高 ,持续 2 4h。内毒素和NO的合成抑制剂同时给予时 ,ET - 1的浓度高于单纯内毒素组。内毒素和NO的合成底物同时给予时 ,ET - 1的浓度低于单纯内毒素组。内毒素和ET - 1抗体同时给予时 ,NO的浓度高于单纯内毒素组。 结论 内毒素可使血管内皮细胞合成并释放ET - 1和NO增加。NO部分抑制ET - 1的合成和释放 ;ET - 1则促进NO的合成和释放。
Objective To study the dynamic changes of the c on centration of plasmatic and hepatic endothelin-1 (ET-1) and nitric oxide (NO) in endotoxic rats. Methods One hundred and fifty rats were randomly divided into control, endotoxin, endotoxin plus L-arginine, endotoxin plus nitric-L-argin ine, endotoxin plus ET-1 antibody groups. The changes of plasmatic and hepatic ET-1 and NO were measured at 3rd, 6th, 9th, 12th, 24th hours after endotoxi n administration. Results After endotoxin administration, the concentration of plasmatic, hepatic ET-1 was significantly increased at 3rd hour (P<0.01), a nd was still higher than the normal level at 24 hour (P<0.05～0.01). Administr ation of nitric-L-arginine, an inhibitor of nitric oxide synthase, increased t he endotoxin-induced ET-1 release. NO production with L-arginine remarkably i nhibited the endotoxin-induced ET-1 release. The concentration of plasmatic, h epatic NO was higher in endotoxin plus ET-1 antibody group than in endotoxin gr oup (P<0.05～0.01). Conclusions It suggests that endotoxin may lead to the increa se of ET-1 and NO in synthesis and release. NO may inhibit in part ET-1 synthe sis and release, while ET-1 increase the production of NO.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2001年第3期166-168,共3页
Chinese Journal of Trauma
基金
全军重点实验室课题资助项目 (1997卫科训字第 71号 )
