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[大鼠椎动脉和颈动脉闭塞诱导短暂性脑缺血后局部血液灌注不足及能量代谢的演变]

[Evolution of the regional blood deficit and energy metabolism after induction of transient cerebral ischemia by occlusion of the vertebral and carotid arteries in the rat].

作者信息

Marie C, Bralet J

出版信息

C R Seances Soc Biol Fil. 1984;178(4):487-92.

PMID:6241021
Abstract

A transient brain ischemia of 10 min duration was produced in rats by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. Ischemia reduced blood flow to 10-18% of the control values in forebrain structures (cortex, striatum, thalamus) and to 25-50% in the mesencephalon, cerebellum and brain stem. In these last structures, after 30 min of recirculation, the flow rates returned to normal values but a 20-35% reduction of blood flow was present in the forebrain structures, indicating that the development of the postischemic hypoperfusion was related to the severity of the preceding ischemia. After 30 min of recirculation, there was a near complete recovery of the high energy compounds but a residual metabolic dysfunction was evidenced by an increase in lactate/pyruvate ratio and an elevation of the glucose content, suggesting a depression of cerebral metabolism which may account for the brain hypoperfusion.

摘要

通过电灼椎动脉和可逆性阻断颈动脉,在大鼠中造成持续10分钟的短暂性脑缺血。缺血使前脑结构(皮质、纹状体、丘脑)的血流降至对照值的10 - 18%,中脑、小脑和脑干的血流降至对照值的25 - 50%。在这些最后的结构中,再灌注30分钟后,血流速率恢复到正常值,但前脑结构中存在20 - 35%的血流减少,这表明缺血后低灌注的发展与先前缺血的严重程度有关。再灌注30分钟后,高能化合物几乎完全恢复,但乳酸/丙酮酸比值增加和葡萄糖含量升高证明存在残余的代谢功能障碍,提示脑代谢抑制,这可能是脑低灌注的原因。

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