Extracellular potassium in a neocortical core area after transient focal ischemia
Extracellular potassium in a neocortical core area after transient focal ischemia
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DOI：
10.1161/01.str.28.1.206
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发表时间：
1997-01-01
期刊：
影响因子：
8.3
通讯作者：
Siesjo, BK
中科院分区：
文献类型：
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作者：
Gido, G;Kristian, T;Siesjo, BK
背景与目的大脑中动脉（MCAO）闭塞导致密集缺血核心区生物能量衰竭。在再灌注期间，生物能量状态的短暂恢复随后是二次恶化。在这项研究中，我们记录了MCAO 2小时内皮质核心的细胞外钾浓度，以及恢复期间。一组动物循环周期为6 ~ 8小时，给予自由基自旋诱捕剂α -苯基- n -叔丁基硝基（PEN）。方法以成年雄性Wistar大鼠（305 ~ 335 g）为实验对象。通过腔内纤维技术闭塞右MCA。对于[K+](e)测量，在右侧皮质上开颅，将离子敏感微电极置入缺血病灶。[K+](e)持续记录2小时。再灌注48小时后，用2,3,5-三苯四氮唑估计梗死面积。结果中动脉闭塞时，[K+](e)升高至约60 mmol/L。然而，一些动物表现出短暂的（和部分的）复极期，并伴有[K+](e)的减少。再灌注后，[K+](e)立即开始恢复，并在3 ~ 5分钟内达到基线水平（2.5 mmol/L）。在恢复的前6小时，[K+](e)稳定在2.5 mmol/L左右，但在此之后，[K+](e)出现了适度的增加。在再灌注1小时后注射PEN的动物中未观察到这种情况。数据表明，迟发性细胞膜功能障碍发生在再灌注约6小时后，表现为[K+](e)升高，单剂量PEN治疗可改善或延缓这种质膜功能恶化。
Background and Purpose Occlusion of the middle cerebral artery (MCAO) results in bioenergetic failure in the densely ischemic core areas. During reperfusion, transient recovery of the bioenergetic state is followed by secondary deterioration. In this study, we recorded the extracellular potassium concentrations in the cortical core during 2 hours of MCAO, as well as during recovery. One group of animals with recirculation periods of 6 to 8 hours was given the free radical spin trap alpha-phenyl-N-tert-butyl nitrone (PEN).Methods The experiments were performed on adult male Wistar rats (305 to 335 g). The right MCA was occluded by an intraluminal filament technique. For [K+](e) measurements a craniotomy was made over the right cortex, and an ion-sensitive microelectrode was lowered into the ischemic focus. Recording of [K+](e) was continued for 2 hours. After 48 hours of reperfusion, infarction size was estimated with 2,3,5-triphenyltetrazolium chloride.Results During MCA occlusion, [K+](e) rose to approximate to 60 mmol/L. However, several animals showed transient (and partial) periods of repolarization accompanied by a decrease in [K+](e). Immediately on reperfusion, the [K+](e) started to recover and reached baseline levels (2.5 mmol/L) within 3 to 5 minutes. During the first 6 hours of recovery, [K+](e) was stable at about 2.5 mmol/L, but after this period a moderate increase in the [K+](e) was observed. This was not observed in animals injected with PEN 1 hour after reperfusion.Conclusions The data suggest that delayed cell membrane dysfunction, as reflected in a rise in [K+](e), occurs after about 6 hours of reperfusion and that treatment with PEN in a single dose ameliorates or delays such deterioration of plasma membrane function.