Gidö G, Kristián T, Siesjö B K
Laboratory for Experimental Brain Research, University Hospital, Lund, Sweden.
Stroke. 1997 Jan;28(1):206-10. doi: 10.1161/01.str.28.1.206.
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 (PBN).
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.
During MCA occlusion, [K+]e rose to approximately 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 PBN 1 hour after reperfusion.
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 PBN in a single dose ameliorates or delays such deterioration of plasma membrane function.
大脑中动脉闭塞（MCAO）会导致严重缺血核心区域出现生物能量衰竭。在再灌注期间，生物能量状态短暂恢复后会继发恶化。在本研究中，我们记录了MCAO 2小时期间以及恢复过程中皮质核心区域的细胞外钾浓度。一组再循环时间为6至8小时的动物给予自由基自旋捕获剂α-苯基-N-叔丁基硝酮（PBN）。
实验在成年雄性Wistar大鼠（305至335克）身上进行。采用腔内丝线技术闭塞右侧大脑中动脉。为测量细胞外钾浓度（[K+]e），在右侧皮质进行开颅手术，并将离子敏感微电极插入缺血灶。持续记录[K+]e 2小时。再灌注48小时后，用氯化三苯基四氮唑评估梗死面积。
在MCA闭塞期间，[K+]e升至约60 mmol/L。然而，几只动物出现了短暂（且部分）的复极化期，伴随着[K+]e的下降。再灌注即刻，[K+]e开始恢复，并在3至5分钟内达到基线水平（2.5 mmol/L）。在恢复的前6小时，[K+]e稳定在约2.5 mmol/L，但在此之后观察到[K+]e有适度升高。在再灌注1小时后注射PBN的动物中未观察到这种情况。
数据表明，再灌注约6小时后会出现延迟的细胞膜功能障碍，表现为[K+]e升高，且单次剂量的PBN治疗可改善或延迟这种质膜功能恶化。
