慢性脑低灌注动物模型再探讨

目的 建立一种新的慢性脑低灌注动脉模型，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 24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。

Development of a new animal model with chronic cerebral hypoperfusion

Objective A new animal model of chronic cerebral hypoperfusion was created to study the effect of the arterial and venous circulation on cerebral perfusion pressure(CPP), and the pathological changes in brain during restoration of normal perfusion pressure.Methods 24 Sprague Dawley rats were randomly assigned to model group, arteriovenous fistula (AVF) group and sham operation group. Animals in model group were accomplished by end to side anastomosis between the right external jugular vien and commod carotid artery, as well as ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Mean arterial pressure(MAP), drainage vein pressure(DVP) and CPP were monitored among the three groups preoperatively, intraoperatively and 3 months after operation. Blood brain barrier(BBB) disruption and water content in rat brains were quantified.The ultramicro structure of the brain was observed under transmission electron microscopy (TEM) after occlusion of arteriovenous fistula. Results Arteriovenous shunt resulted in decreased MAP, increased DVP and decreased CPP significantly. Three months later, there were also increased DVP and decreased CPP significantly compared with that of the other groups. Damage to the BBB and brain edema were noted in animals of the model group after occlusion of AVF. TEM revealed vasogenic brain edema and (/or) hemorrhage in various degrees, which related to absent astrocytic foot processes around some cerebral capillaries. Conclusions Carotid jugular end to side anastomosis can induce decreased CPP, whereas further cerebral hypoperfusion states maybe caused by drainage vein abnormalities, which are associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.