小鼠不完全性脑缺血、再灌注时脑膜血流量的变化及尼莫地平的作用

目的：观察双侧颈总动脉阻断后脑血流的变化。方法：结扎双侧颈总动脉观察小鼠不完全性脑缺血及其再灌注时脑膜血流量的变化。结果：结扎颈总动脉后小鼠脑膜血流量在几秒钟内骤然下降，血流量较结扎前降低约８５．９％±６．４５％。同时血管中红细胞运动近停滞状态，血管再通时脑血流处于低灌注状态，血流量下降３４．４７％±１１．６９％，此时脑缺血再灌后脑组织实际上处于一种慢性缺血状态。再灌注１０ｄ后，小鼠脑海马ＣＡ１区神经细胞数明显减少。尼莫地平可以解除再灌注时的脑血流低灌状态。并防止由此所引起的脑海马ＣＡ１区神经细胞的缺失。结论：缺血后及时给予尼莫地平具有积极的治疗意义。

Miningeal blood flow by incomplete reansient cerebral ischemia reperfusion and the effect of nimodipine in mice

AIM: To observe the miningeal blood blow by incomplete reansient cerebral ischemia reperfusion and the effect of nimodipine in mice. METHODS: By the way of ligaturing the cephalic arteries to observe the miningeal blood flow. RESULTS: Forebrain blood flow of mice decreased sharply in a few seconds as soon as ligaturing the cephalic arteries, which the blood was 85 94%±6 45% downwards, compared with normal mice. Meanwhile, the movement of the red blood cells in the vessles stopped nearly. After 5 min, the arteries untied off, the blood was 34 47%±11 69% downwards in lower level showing that the cerebral tissue was in fact in the condition of chronic poor blood reperfusion at that time. After 10 days of the reperfusion, the number of neurons in field CA 1 of Ammons horn, which had the relation of the learning and memory, decreased. Nimodipine (100 mg·kg -1 ,iv) could modify this reperfusion in lower level and protect the neurons from the injury. CONCLUSIONS: Suggesting, giving nimodipine to the patient just after cerebral ischemia in clinic as soon as possible has the active significance.