脑缺血中的脑离子稳态。

A J Hansen, M Nedergaard
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引用次数: 131

摘要

缺血时脑功能受到严重干扰。在几秒钟内,意识和自发活动消失,而间质主要离子的浓度保持在正常水平附近。几分钟后,钾急剧增加,钠、氯和钙浓度降低。类似的离子变化在扩张性抑郁期间也被观察到,然而,这种变化是自发可逆的,并且可能在正常灌注的大脑中引起。局灶性缺血时,这两种情况同时发生。非常低流量的中央核心表现为间质钾浓度的缺血性增加,而周围组织则表现为反复发作的扩张性抑制。这可能通过刺激血流抑制区域的代谢从而引起缺血核心外的细胞损伤而诱发能量衰竭。
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Brain ion homeostasis in cerebral ischemia.

Brain function is severely disturbed in ischemia. Within seconds, consciousness and spontaneous activity is lost, whereas interstitial concentrations of major ions are kept near normal levels. After a few minutes, there is a dramatic increase of potassium and a lowering of sodium, chloride, and calcium concentrations. Similar ionic changes are observed during spreading depression, however, that is spontaneously reversible and may be elicited in the otherwise normally perfused brain. In focal ischemia, the two events occur simultaneously. The central core of very low flow displays the ischemic increase of interstitial potassium concentration, whereas the surrounding tissue exhibits repeated episodes of spreading depression. This may induce energy failure by stimulating metabolism in areas with depressed flow thereby causing cell damage outside the ischemic core.

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The mechanism of ischemia-induced brain cell injury. The membrane theory. Peroxidative damage to cell membranes following cerebral ischemia. A cause of ischemic brain injury? Phosphoinositide turnover and calcium ion mobilization in receptor activation. Polyamines in cerebral ischemia. Reduction of neural damage in irreversible cerebral ischemia by calcium antagonists.
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