Relation of postischemic delayed hypoperfusion and cerebral edema after transient forebrain ischemia.
Relation of postischemic delayed hypoperfusion and cerebral edema after transient forebrain ischemia.
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DOI：
10.1016/j.jstrokecerebrovasdis.2006.12.001
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发表时间：
2007-05-01
期刊：
影响因子：
--
通讯作者：
Kohno, Masakazu
中科院分区：
文献类型：
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作者：
Hosomi, Naohisa;Ohyama, Hideo;Kohno, Masakazu
缺血后迟发性低灌注（PDH）是基于局部血管舒张剂和血管收缩剂之间的失衡。我们评估了麻醉沙鼠双侧颈总动脉闭塞引起短暂性前脑缺血后脑血流量和脑比重的时间过程，以确定PDH是否是脑水肿发展的重要因素。再灌注后45分钟出现PDH，随后脑水肿加重。此后，尽管脑比重稳定，但再灌注后24小时局部脑血流量从PDH恢复。此外，在3种不同的脑缺血持续时间（30、60和90分钟）中，脑比重与再灌注120分钟后的局部脑血流量建立了线性相关性。提示脑水肿不是PDH发生的原因，但PDH可引起脑水肿。
Postischemic delayed hypoperfusion (PDH) is based on the imbalance between local vasodilators and vasoconstrictors. We evaluated the time course of cerebral blood flow and cerebral specific gravity representing cerebral edema after transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils to determine whether PDH is a significant factor in development of cerebral edema. PDH appeared 45 minutes after reperfusion followed by the increase of cerebral edema. Thereafter, the local cerebral blood flow recovered from PDH 24 hours after reperfusion in spite of the stable cerebral specific gravity. Furthermore, cerebral specific gravity established a linear correlation with the local cerebral blood flow 120 minutes after reperfusion in the 3 different durations of cerebral ischemia (30, 60, and 90 minutes). It is suggested that cerebral edema is not the cause in PDH development, but PDH may cause cerebral edema.