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单侧颈动脉闭塞后中度症状性沙鼠的缺血耐受性。

Ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion.

作者信息

Kitagawa K, Matsumoto M, Matsushita K, Mandai K, Mabuchi T, Yanagihara T, Kamada T

机构信息

First Department of Internal Medicine, Osaka University Medical School, Japan.

出版信息

Brain Res. 1996 Apr 15;716(1-2):39-46. doi: 10.1016/0006-8993(96)00023-6.

Abstract

Ischemic tolerance following transient global cerebral ischemia has drawn considerable attention because of the putative cell defense mechanism which may be inducible by ischemic stress. The purpose of this study is to investigate the inducibility of ischemic tolerance in moderately symptomatic gerbils after unilateral carotid occlusion. Adult Mongolian gerbils were used. Under ether inhalation, the right common carotid artery was occluded for up to 30 min with an aneurysmal clip. Immediately after occlusion, neurological signs and motor function were evaluated and gerbils with moderate signs were selected for investigation of ischemic tolerance. Ischemia for 30 min to gerbils with moderate signs constantly caused neuronal death in the caudoputamen, but it was prevented by pretreatment with 10 min ischemia which was reversible but strong enough to produce heat shock protein 70. The results show that ischemic tolerance can be induced after hemispheric cerebral ischemia as in the case of global cerebral ischemia and suggest that ischemic tolerance may be relevant in human stroke.

摘要

短暂性全脑缺血后的缺血耐受由于可能由缺血应激诱导的假定细胞防御机制而备受关注。本研究的目的是探讨单侧颈动脉闭塞后中度症状性沙鼠缺血耐受的诱导情况。使用成年蒙古沙鼠。在吸入乙醚的情况下,用动脉瘤夹将右侧颈总动脉闭塞长达30分钟。闭塞后立即评估神经体征和运动功能,选择有中度体征的沙鼠进行缺血耐受研究。对有中度体征的沙鼠进行30分钟缺血会持续导致尾壳核神经元死亡,但通过10分钟缺血预处理可预防,该预处理虽可逆但强度足以产生热休克蛋白70。结果表明,半球性脑缺血后可诱导缺血耐受,如同全脑缺血的情况,提示缺血耐受可能与人类中风相关。

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