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在既往研究大鼠蛛网膜下腔出血（SAH）后局部脑血流量（rCBF）变化的基础之上，进一步观察SAH后颅底血管痉挛状态和结构变化、血脑屏障（BBB）开放及脑水肿过程．发现SAH后颅底动脉出现间期为72h的痉挛过程，rCBF变化与之有显著的相关性（r＝0．93，P＜0.01）；SAH后早期血管壁呈现强烈的收缩，无血管壁结构变化，晚期在血管壁扩张过程中有部分内皮细胞脱落，弹力膜断裂和平滑肌细胞退性变；SAH后早中期出现轻度BBB通透性增加和脑水肿，二者之间有显著的相关性（r＝0．92，P＜0．01）；BBB通透性改变与血管痉挛有显著的负相关关系（r＝－0．84，p＜005）．这些结果提示：SAH后rCBF变化是反映脑血管痉挛（CVS）状态的较好功能指标；SAH后CVS主要是由脑血管收缩功能改变所致而非血管壁结构改变所致；SAH后出现轻度的BBB开放和血管源性脑水肿，主要是由于CVS引起，但也可能间接部分地影响CVS过程。
On the basis of previous studies on the changes of regional cerebral blood flow (rCBF) after subarachnoid hemorrhage (SAH) in rats, we further observed the changes in the status and structure of cranial base vasospasm, the opening of the blood-brain barrier (BBB) and the brain edema process. It was found that there was a significant correlation between rCBF and the changes of rCBF in the basilar artery of SAH after 72h (r = 0.93, P <0.01). In the early stage of SAH, there was a strong contraction of the vessel wall without vessel wall structure Changes in advanced vascular wall during the expansion of some endothelial cells shedding, stretch membrane rupture and smooth muscle cell degeneration; early post-SAH mild BBB increased permeability and cerebral edema, there was a significant correlation between the two (R = 0.92, P <0.01). There was a significant negative correlation between BBB permeability changes and vasospasm (r = -0.84, p <005). These results suggest that the change of rCBF after SAH is a good function index reflecting the state of cerebral vasospasm (CVS). After SAH, CVS is mainly caused by the change of cerebrovascular contractile function rather than the change of vascular wall structure. BBB opening and vasogenic brain edema are mainly caused by CVS, but may also indirectly affect the CVS process indirectly.