兔大脑缺血再灌流新模型

A new model of global postischemic reperfusion in rabbit

本文报道了兔大脑缺血再灌流新模型。方法为结扎双侧椎动脉(VA),同时可逆性阻断双侧颈内动脉(ICA)和双侧颈外动脉(ECA),即6-动脉阻断(6AO),60分钟后复流双侧ICA和ECA 120分钟。实验结果显示,脑电活动明显受抑制,脑组织含水量增加至80.41±0.82%,对照组78.13±0.53%((?)±SD),P<0.01。超微结构提示在缺血60分钟时有细胞毒性脑水肿存在,当再灌流120分钟时,细胞毒性和血管源性脑水肿同时存在。与传统的双侧VA和和颈总动脉(CCA)阻断(4AO)模型比较,6AO造成的再灌流损伤较4AO方法更为严重,且不必同时降低全身血压,避免了低血压造成其他重要脏器损伤的可能性。

The present study describes a new model of global postischemic reperfusion characterized by lack of systemic hypotension. The experimental precedure involves reversible occlusion of the bilateral internal carotid arteries (ICA) and bilateral external carotid arteries (ECA) for 60 minutes combined with permanent ligation of bilateral vetebral arteries (VA), i. e. 6-artery occlusion (6AO). Sixty minutes after the occlusion, bilateral ICA and ECA were released for 120 minutes at which time the experiment was terminated. The results revealed severely depressed EEG activity; water content of brain tissue increased to 80.41±0.82% (control 78.13±0.53%, P<0.01). The ultrastructure revealed that cytotoxic brain edema was present at 60 minutes of ischemia, and both cytotoxic and vasogenic brain edema occurred after 120 minutes of reperfusion. To estimate the effect of 6AO injection of 1% Evans blue into the ascending aorta revealed the severe imcomplete ischemia of bilateral hemispheres was induced by 6AO. These results were compared with those obtained with the model of 4-artery (bilateral common carotid arteries and VAs) occlusion (4AO), and suggested that the brain damage was more severe with 6AO than with 4AO.