内毒素血症大鼠脑底动脉内皮素-1能神经纤维表达与分布的变化

目的:探讨内毒素血症大鼠脑底动脉内皮素-1(ET-1)能神经纤维诱发脑血管痉挛发生与发展的关系,为深入阐明内毒素血症诱发脑血管痉挛的发病机制提供形态学依据。方法:96只Wistar大鼠随机分为对照组、内毒素血症组(注射内毒素第3、6、12、24、48h),分别采用放射免疫法检测血浆内皮素-1水平的变化,采用免疫组织化学ABC法对大鼠脑底动脉内皮素-1能神经纤维进行观察。结果:内毒素血症后3、6、12h大鼠血浆内皮素-1水平较对照组明显升高(P0.05),内毒素血症后24h和48h已趋于正常(P0.05)。此外,对照组和内毒素组大鼠脑底动脉可见棕褐色,呈细线状分布的内皮素-1能免疫反应阳性纤维,其中内毒素血症后第6h和12h大鼠脑底动脉内皮素-1能神经纤维密度显著增高(P0.05)。结论:内毒素血症大鼠血浆内皮素-1水平升高,脑底动脉内皮素-1能神经纤维密度增加,提示内皮素-1参与了内毒素血症诱发脑血管痉挛的病理生理过程,为脑血管痉挛的神经-体液调节机制提出了新思路,同时为临床预防和治疗脑血管痉挛提供了理论依据。

The change of expression and distribution of endothelin-1 immunoreactive nerve fibers on cerebral arteries in endotoxemia rats

Objective:To investigate the relationship between endotoxemia-induced cerebral vasospasm and endothelin-1 (ET-1) innervation on cerebral arteries,and to provide a morphological data for illuminating the pathogenesis of endotoxemia-induced cerebral vasospasm in endotoxemia rats.Methods:96 Wistar rats were randomly divided into control group and experimental group,the latter was then subdivided into 3,6,12,24 and 48 h groups after the injection of lipopolysaccharide (LPS).The change of plasma ET-1 was detected by radioimmunoassay technique,and ET-1 immunoreactive nerve fibers on cerebral arteries were examined with immunohistochemistry and measured with stereoscopy method.Results:LPS treatment caused a significant increase of plasma ET-1 at 3,6 and 12 h after LPS injection when compared to the control group (P<0.05).However in 24 h and 48 h LPS-treated groups,the plasma concentration of ET-1 decreased nearly to the normal level (P>0.05).The ET-1 immunoreactive nerve fibers were observed in all groups,which were of brown color and thin.Moreover,at 6 h and 12 h after LPS treatment,the density of ET-1 immunoreactive nerve fibers on cerebral arteries was much higher than that of control group (P<0.05).Conclusion:The endotoxemia induced the increase of ET-1 in blood plasma,and enhanced the density of ET-1 immunoreactive cerebral arterial nerve fibers.It indicated that ET-1 played an important role in the development of cerebral vasospasm induced by endotoxemia.The results provided a theoretical basis for the neurohumoral modulation mechanism of cerebral vasospasm.