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机构地区:[1]南昌大学医学院脑血管研究所解剖学教研室,南昌330006
出 处:《神经解剖学杂志》2010年第3期289-293,共5页Chinese Journal of Neuroanatomy
基 金:江西省自然科学基金项目(2009GZY0134)
摘 要: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(P<0.05),内毒素血症后24h和48h已趋于正常(P>0.05)。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(P<0.05)。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。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 endo- toxemia-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 immunoreaetive 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.
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