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缺血后高氧增强兔脊髓缺血模型的易损性。

Postischemic hyperoxia enhances vulnerability in the rabbit spinal cord ischemic model.

机构信息

Institute of Neurobiology, Slovak Academy of Sciences, Kosice (Czechoslovakia).

出版信息

Restor Neurol Neurosci. 1992 Jan 1;3(6):283-91. doi: 10.3233/RNN-1992-3601.

Abstract

This study evaluated whether or not reperfusion of the rabbit ischemic spinal cord under conditions of varying blood oxygen tension combined with low blood viscosity can alter the neurological outcome after 15 min of infrarenal aortic occlusion. In group A (n = 20), hyperoxic reperfusion was performed during the initial 30 min of recirculation (pO2 = 460 ± 72 mmHg). In group B (n = 20), no attempt was made to manipulate the physiological arterial pO2 tension. In group C (n = 20), graded postischemic reoxygenation was applied during 15 min of recirculation beginning with 48 ± 12 mmHg as the initial arterial pO2. Neurological analysis revealed a high incidence of paraplegic animals after hyperoxic reperfusion as opposed to relatively undamaged animals after normoxic or graded postischemic reoxygenation. The possible role of different pathobiochemical events, specifically the high molecular oxygen availability and oxygen free-radical overproduction, is discussed below with attention to the interneuronal destructive process, detected during the early reoxygenation phase by means of the Nauta method permitting the visualization of the early signs of somatic and dendritic argyrophilia.

摘要

本研究旨在评估在不同血氧分压条件下对兔缺血性脊髓进行再灌注,同时降低血液黏度,是否会改变肾下主动脉阻断 15 分钟后的神经功能结局。在 A 组(n = 20)中,在再灌注的最初 30 分钟内进行高氧再灌注(pO2 = 460 ± 72 mmHg)。在 B 组(n = 20)中,未尝试操纵生理动脉 pO2 张力。在 C 组(n = 20)中,在再灌注的 15 分钟内开始进行分级的缺血后再氧合,初始动脉 pO2 为 48 ± 12 mmHg。神经学分析显示,高氧再灌注后截瘫动物的发生率很高,而在正常氧合或分级缺血后再氧合后,动物的损伤相对较小。下文将讨论不同的病理生物化学事件的可能作用,特别是高氧分子的可用性和氧自由基的过度产生,同时注意到在早期再氧合阶段通过 Nauta 法检测到的神经元破坏性过程,该方法允许可视化体和树突嗜银性的早期迹象。

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