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目的 探讨内皮素 1(endothelin 1,ET 1)在脑血管痉挛中的作用及其信号传导机制。方法 在建立犬脑血管痉挛动物模型基础上应用免疫生化技术直接对脑基底动脉血管ET 1生物活性和血管平滑肌细胞PKC活性进行检测。同时 ,应用体外血管张力性研究方法进一步观察了ET 1以及ETA 受体阻断剂BQ12 3 和ETA/ETB 受体阻断剂TAK0 4 4对血管张力的作用。结果 造影显示脑血管痉挛程度与PKC激活程度密切相关 ,基底动脉血管ET 1免疫生物活性仅仅在脑血管痉挛早期一过性增高 ,体外实验显示ET 1具有强烈的致血管痉挛和明显激活PKC作用 ,这种作用能被ET受体阻断剂BQ12 3和TAK0 4 4明显阻断。结论 ET 1仅仅在脑血管痉挛早期起致血管痉挛作用 ,这种作用是通过ET受体启动、激活PKC而实现的 ,而在维持脑血管痉挛过程中ET 1不起主要作用
Objective To investigate the role of endothelin 1 (ET 1) in cerebral vasospasm and its signal transduction mechanism. Methods The biological activity of ET 1 and the activity of PKC in vascular smooth muscle cells of cerebral basilar artery were detected by immunobiochemical technique based on animal models of canine cerebral vasospasm. At the same time, the effect of ET 1 and ETA receptor blockers BQ12 3 and ETA / ETB receptor antagonist TAK0 4 4 on vascular tone was further observed by in vitro vascular tension study. Results Angiography showed that the degree of cerebral vasospasm was closely related to the activation of PKC. The immunological activity of ET 1 in basilar artery was transiently elevated only in the early stage of cerebral vasospasm. In vitro experiments showed that ET 1 had a strong vasoconstriction and activation of PKC. This effect was significantly blocked by the ET receptor blockers BQ12 3 and TAK0 4 4. Conclusions ET 1 causes vasospasm only in the early stage of cerebral vasospasm. This effect is initiated by activating ET receptors and activating PKC, whereas ET 1 does not play a major role in maintaining vasospasm