论文部分内容阅读
目的 建立一种新的慢性脑低灌注动物模型 ,研究动脉和静脉循环对脑灌注压 (CPP)的影响及正常灌注压恢复时脑组织病理变化。方法 2 4只SD大鼠随机分为模型组、动静脉瘘 (AVF)组和假手术组。模型组动物行右侧颈外静脉 颈总动脉端侧吻合 ,同时结扎左侧横窦引流静脉及双侧颈外动脉。分别于术前、术后即刻和术后 3个月检测各组动物平均动脉压 (MAP)、颅内引流静脉压(DVP)和CPP。 3个月后阻断AVF ,定量检测血脑屏障 (BBB)破坏程度和脑水含量。透射电镜观察脑组织超微结构。结果 动静脉分流术后MAP明显下降 ,DVP明显升高 ,CPP明显降低。术后 3个月 ,模型组动物DVP仍明显升高 ,CPP明显降低 ,与其他两组动物相比差别有显著性。AVF阻断后模型组动物BBB明显破坏 ,脑水含量明显增加。电镜证实脑组织中有不同程度的血管源性脑水肿和(或 )出血 ,并与脑部分毛细血管周围星形胶质细胞足突消失有关。结论 颈动静脉端侧吻合可导致CPP降低 ,静脉引流障碍进一步加重脑低灌注状态 ,并与灌注压突破密切相关。该动物模型符合人脑动静脉畸形的基本血流动力学特征
Objective To establish a new animal model of chronic cerebral hypoperfusion to study the effect of arterial and venous circulation on cerebral perfusion pressure (CPP) and the pathological changes of brain tissue during normal perfusion pressure recovery. Methods 24 SD rats were randomly divided into model group, AVF group and sham operation group. Animals in the model group were performed anastomosis of the common carotid artery on the right side of the external jugular vein while ligating the left transverse sinus drainage vein and bilateral external carotid artery. The mean arterial pressure (MAP), intracranial drainage venous pressure (DVP) and CPP of each group were measured before operation, immediately after operation and 3 months after operation. After 3 months, AVF was blocked, and the degree of BBB destruction and brain water content were quantitatively detected. TEM observation of ultrastructure of brain tissue. Results MAP decreased significantly after arteriovenous shunt, DVP increased significantly, CPP decreased significantly. At 3 months after operation, the DVP in model group was still significantly higher and CPP was significantly lower than that in the other two groups. After the AVF block, BBB in the model group was obviously destroyed, and the brain water content increased obviously. Electron microscopy confirmed the presence of varying degrees of vasogenic brain edema and / or hemorrhage in the brain and was associated with the disappearance of astrocytes around the capillaries in the brain. Conclusions End-to-end anastomosis of the carotid artery leads to a decrease in CPP. Impaired venous drainage further aggravates cerebral hypoperfusion, which is closely related to the breakthrough of perfusion pressure. The animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations