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灵长类动物皮层缺血诱导的细胞外钾变化的可逆性

Reversibility of ischaemically induced changes in extracellular potassium in primate cortex.

作者信息

Branston N M, Symon L, Strong A J

出版信息

J Neurol Sci. 1978 Jun;37(1-2):37-49. doi: 10.1016/0022-510x(78)90226-5.

Abstract

Following the massive increase in extracellular potassium activity that occurs in cerebral cortex when local blood flow falls below 8--11 ml/100 g/min, recovery of potassium toward normal levels might be expected when flow is restored. This study assessed the reversibility of such potassium increases, produced by middle cerebral artery occlusion in 13 baboons anaesthetised with alpha-chloralose, in relation to a wide range of ischaemic duration and density and post-occlusion flow. Potassium was measured with ion-exchanger microelectrodes and flow by hydrogen clearance. The artery was occluded for 136 +/- 63 min (mean +/- SD) and measurements were continued thereafter for 93 +/- 57 min without systemic hypertension. Upon reperfusion, partial or complete recovery (i.e., to within control confidence limits) of potassium was seen in all animals, but the rate of recovery varied widely and potassium clearance showed bi-compartmental characteristics in 7 animals. The fast component (or initial slope) rate constant was significantly correlated with post-occlusion flow and (inversely) with the duration of occlusion for which flow fell below the arbitrary threshold of 10 ml/100 g/min (the flow deficit). The slow component was unrelated to these quantities. Complete recovery was associated with a significantly higher post-occlusion flow, and smaller flow deficit, than was partial recovery. Secondary increases in potassium, associated with relatively high flow deficits and post-occlusion flows, were seen in 5 animals. These results are discussed in terms of factors that may determine potassium clearance and the possibility that elevated levels of potassium (demonstrated here to be prolonged well into the post-occlusion phase) might influence the evolution of a cortical infarct.

摘要

当局部脑血流降至8 - 11 ml/100 g/min以下时,大脑皮层细胞外钾离子活性会大幅增加。当血流恢复时,钾离子有望恢复至正常水平。本研究评估了13只经α-氯醛糖麻醉的狒狒大脑中动脉闭塞后产生的钾离子增加的可逆性,该可逆性与广泛的缺血持续时间、缺血密度以及闭塞后血流情况相关。采用离子交换微电极测量钾离子,通过氢清除法测量血流。动脉闭塞136 ± 63分钟(均值±标准差),此后在无全身性高血压的情况下继续测量93 ± 57分钟。再灌注时,所有动物的钾离子均出现部分或完全恢复(即恢复至对照置信区间内),但恢复速率差异很大,7只动物的钾离子清除显示出双室特征。快速成分(或初始斜率)速率常数与闭塞后血流显著相关,且与血流降至任意阈值10 ml/100 g/min以下(血流不足)的闭塞持续时间呈负相关。缓慢成分与这些量无关。完全恢复与闭塞后血流显著更高、血流不足更小相关,相比之下部分恢复则不然。5只动物出现了与相对较高的血流不足和闭塞后血流相关的钾离子继发性增加。本文根据可能决定钾离子清除的因素以及钾离子水平升高(在此显示在闭塞后阶段会持续很长时间)可能影响皮质梗死演变的可能性对这些结果进行了讨论。

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