Hai Jian, Ding Meixiu, Guo Zhilin, Wang Bingyu
Department of Neurosurgery, Tongji Hospital, Tongji University, Shanghai, People's Republic of China.
J Neurosurg. 2002 Nov;97(5):1198-202. doi: 10.3171/jns.2002.97.5.1198.
A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure.
Twenty-four Sprague-Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ipsilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood-brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries.
The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.
建立一种新的慢性脑灌注不足实验模型，以研究全身动脉分流和颅内静脉血引流主要血管阻塞对脑灌注压（CPP）的影响，以及恢复正常灌注压后脑的病理变化。
将24只Sprague-Dawley大鼠随机分为假手术组、动静脉瘘（AVF）组和模型组（每组8只）。通过右颈外静脉（EJV）远端与同侧颈总动脉（CCA）端侧吻合建立瘘管，随后结扎引流横窦的左静脉和双侧颈外动脉，制备动物模型。术前、术后即刻及90天后监测并比较三组的全身平均动脉压（MAP）、引流静脉压（DVP）和CPP。90天后瘘管闭塞，通过透射电子显微镜确认并量化大脑中动脉区域右侧皮质组织的血脑屏障（BBB）破坏和含水量。形成瘘管导致AVF组和模型组的MAP和CPP显著降低，DVP显著升高。90天后，与其他组相比，模型组的DVP仍显著升高，CPP显著降低（p<0.05）。在通过闭塞瘘管恢复正常灌注压的过程中，模型组动物出现BBB损伤和脑水肿。电子显微镜研究显示不同程度的脑血管源性水肿和/或出血，这与一些脑毛细血管周围星形胶质细胞足突缺失有关。
结果表明，EJV远端与CCA端侧吻合可导致CPP降低，而静脉流出受限可能导致进一步的慢性脑灌注不足状态，这与灌注压突破有关。该动物模型符合人类脑动静脉畸形的基本血流动力学特征。
