利多卡因对完全压迫性缺血后脑脂质过氧化和中性粒细胞活化的影响。

J Lantos, E Röth, G Temes
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引用次数: 0

摘要

研究了利多卡因对短暂性全脑缺血后颈静脉丙二醛浓度反映的脑脂质过氧化的影响,以及外周静脉血样本中多形核白细胞活化的影响。常温犬脑脊液压升高10 min,再灌注60 min后,颈静脉丙二醛浓度在再灌注前3 min显著升高(p < 0.05)。利多卡因(10mg /kg,静脉注射)在缺血前10min,不仅可以阻止丙二醛浓度在缺血期间的升高,而且在再灌注开始后10min也会引起丙二醛浓度的短暂性显著下降。缺血10分钟和再灌注60分钟后,无论是缺血还是添加利多卡因后,多形核白细胞自由基的产生都没有明显变化。这些结果表明,利多卡因对自由基过程有清除作用,但对缺血后再灌注早期多形核白细胞的激活没有直接影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of lidocaine on cerebral lipid peroxidation and neutrophil activation following complete compression ischemia.

The effect of lidocaine on brain lipid peroxidation, as reflected by jugular vein malondialdehyde concentrations, and of polymorphonuclear leukocyte activation in peripheral venous blood samples following transient global cerebral ischemia, were studied. In normothermic dogs subjected to a 10 min elevation of cerebrospinal fluid pressure and a subsequent 60 min reperfusion, the malondialdehyde concentration during the first 3 min of reperfusion increased significantly (p < 0.05) in the jugular vein. Lidocaine (10 mg/kg, i.v.), administered 10 min before ischemia, not only prevented the elevation of the malondialdehyde concentrations during ischemia, but also provoked a significant transient decrease 10 min after the start of reperfusion. A 10 min ischemia and a 60 min reperfusion caused no significant changes in the polymorphonuclear leukocyte radical production, neither following ischemia nor after addition of lidocaine. These results suggest that lidocaine exerts a scavenging action on free radical processes but that it has no direct effect on the polymorphonuclear leukocyte activation in the early phase of reperfusion following ischemia.

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