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大鼠光血栓性大脑中动脉闭塞2小时后,再灌注诱导半暗带出现治疗窗的短暂现象。

Reperfusion-induced temporary appearance of therapeutic window in penumbra after 2 h of photothrombotic middle cerebral artery occlusion in rats.

作者信息

Yao Hiroshi, Yoshii Narihiko, Akira Toshiaki, Nakahara Tatsuo

机构信息

Laboratory for Neurochemistry, Center for Emotional and Behavioral Disorders, National Hospital Organization, Hizen Psychiatric Center, Saga, Japan.

出版信息

J Cereb Blood Flow Metab. 2009 Mar;29(3):565-74. doi: 10.1038/jcbfm.2008.147. Epub 2008 Dec 17.

DOI:10.1038/jcbfm.2008.147
PMID:19088742
Abstract

To explore the effects of reperfusion on evolution of focal ischemic injury, spontaneously hypertensive male rats were subjected to photothrombotic distal middle cerebral artery occlusion (MCAO) with or without YAG laser-induced reperfusion. The volume of fodrin breakdown zone, water content, and brain tissue levels of sodium (Na(+)) and potassium (K(+)) were measured in the ischemic core and penumbra. Reperfusion attenuated fodrin breakdown, and the volume containing fodrin breakdown product at 3 h after reperfusion (5 h after MCAO) (30+/-7 mm(3)) was significantly smaller than the 42+/-3 mm(3) of the permanent occlusion group. After 3 to 6 h of ischemia, Na(+) increased, and K(+) decreased in the ischemic core. Reperfusion after 2 h of MCA occlusion did not mitigate the ischemia-induced changes in brain tissue electrolytes and water content at 3 to 6 h of ischemia. Even in reperfusion after comparatively long periods of occlusion where brain infarction size, assessed 3 days after MCAO, was not significantly reduced by reperfusion, and the precipitating indicators of the ischemic core (Na(+), K(+), water content) did not improve, temporary improvement or a delay in progression of ischemic injury was discernible in the penumbra. These results indicate the possibility that treatment with reperfusion is permissive to the effects of neuroprotection.

摘要

为了探究再灌注对局灶性缺血损伤演变的影响,对自发性高血压雄性大鼠进行光血栓性大脑中动脉远端闭塞(MCAO),并施加或不施加YAG激光诱导的再灌注。测量缺血核心区和半暗带中血影蛋白降解区的体积、含水量以及脑组织中钠(Na⁺)和钾(K⁺)的水平。再灌注减轻了血影蛋白降解,再灌注后3小时(MCAO后5小时)含有血影蛋白降解产物的体积(30±7立方毫米)显著小于永久性闭塞组的42±3立方毫米。缺血3至6小时后,缺血核心区的Na⁺增加,K⁺减少。MCA闭塞2小时后进行再灌注并不能减轻缺血3至6小时后脑组织电解质和含水量的缺血诱导变化。即使在较长时间闭塞后进行再灌注,即MCAO后3天评估的脑梗死体积未因再灌注而显著减小,且缺血核心区的促发指标(Na⁺、K⁺、含水量)也未改善,但在半暗带仍可观察到缺血损伤的暂时改善或进展延迟。这些结果表明再灌注治疗可能具有神经保护作用。

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