目的探讨内皮细胞凋亡在兔蛛网膜下腔出血(SAH)后脑血管痉挛形成中的作用。方法实验分正常组、对照组(枕大池注入生理盐水)、SAH3d组、SAH5d组、SAH7d组和SAH10d组。采用自体动脉血枕大池注入方法建立SAH模型。应用脑血管造影观察基底动脉形态改变,透射电镜和TUNEL技术观察内皮细胞凋亡,免疫组化法检测Caspase-3蛋白表达。结果脑血僻造影发现,SAH后第3天基底动脉狭窄,第7天达高峰,第10天缓解。SAH5d组和SAH7d组丛底动脉壁出现胞浆浓缩、核染色质浓缩边集等凋亡样改变的内皮细胞和较多TUNEL染色阳性内皮细胞,同时内皮细胞中Caspase-3蛋白表达上调,SAH7d组尤为明显;SAH3d组和SAH10d组内皮细胞捌亡样病朋改变减轻,TUNEL染色阳性细胞明显减少,内皮细胞Caspase-3蛋白表达减弱;正常组和对照组术见明显病理改变。结论脑血管壁存在的内皮细胞凋亡可能在SAH后脑血能:痉挛形成中起重要作用。
Objective To explore the role of endothelial eels apoptosis in cerebral vasospasm (CVS) after subarachnoid hemorrhage(SAH). Methods Twenty-four rabbits were divided into 7 groups of normal,control,SAH 3 d,SAH 5 d,SAH 7 d and SAH 10 d. SAH model was produced by injecting autologous arterial blood into the eisterna magna twice at 48-h interval in rabbits. The morphological changes of basilar arteries were studied with angiography. Transmission electron microscopy and TUNEL staining were used to test the endothelial apoptosis in basilar arteries and the expression of Caspase-3 protein was examined with immunohistochemical technique. Results Angiographic vasospasm began on day 3, peaked on day 7 and relieved on day 10 after SAH. Apoptotic-like changes such as condensation of cytoplasm and increased condensation of peripheral chromation, positive staining of TUNEL and upregulation of Caspase-3 protein were observed in endothelial cells in both groups of SAH 5 d and SAH 7 d,espeeially in group SAH 7 d. Conclusion Endothelial apoptosis may play an important role in the development of cerebral vasospasm after SAH.