Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function.
Gro Klitgaard Povlsen, Thomas A Longden, Adrian D Bonev, David C Hill-Eubanks, Mark T Nelson
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引用次数: 0
Abstract
Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.
短暂性全脑缺血后往往会出现迟发性脑血流紊乱，导致神经元损伤。目前对这种紊乱的病理生理过程尚不完全清楚。在这里，我们利用已建立的一过性全脑缺血模型，发现缺血后神经血管耦合显著受损。这种损伤源于实质动脉平滑肌中功能性内向整流钾（KIR）通道的丧失。因此，旨在保护或恢复脑血管 KIR 通道功能的治疗策略可能会改善缺血后的预后。
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