Cumulative effect of repetitive ischemia: pathophysiological findings.

G Nagashima
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Abstract

The cumulative effect of ischemia on the brain was investigated in cats using a repetitive transient global ischemia model. The cats were submitted to three series of repetitive ischemia of 5.0, 7.5 and 10.0-minute durations at 1-hour intervals by intrathoracic clamping of the innominate and subclavian arteries. Pathophysiological changes during and after the ischemic episodes were evaluated by monitoring the electroencephalograms (EEG), cerebral blood flow (CBF), specific gravity and 31P-MR spectroscopy (MRS). Transient 5.0, 7.5, and 10.0-minute ischemias appeared to produce a slightly more severe energy failure on the 31P MRS measurement in the animals that had previously experienced an ischemic injury than those that had not. Additionally, repetition of ischemic episodes at 1-hour intervals led to a progressive lengthening of the duration of the spontaneous electrocortical suppression that followed each ischemic episode. However, preischemic hypoxia (5% O2 for 5 minutes) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate on the MRS measurement, otherwise the EEG activity declined progressively. This shut-down response of the EEG can be concluded to serve in preserving the energy state of the brain although it is not capable of preventing the development of postischemic brain edema and neuronal death.

重复性缺血的累积效应:病理生理学结果。
研究了猫脑缺血的累积效应,采用重复瞬态全脑缺血模型。通过胸内夹持无名动脉和锁骨下动脉,对猫进行5.0、7.5和10.0分钟的重复缺血,间隔1小时。通过监测脑电图(EEG)、脑血流量(CBF)、比重和31P-MR谱(MRS)评估缺血发作期间和之后的病理生理变化。在经历过缺血性损伤的动物中,短暂性缺血5.0分钟、7.5分钟和10.0分钟似乎比没有经历过缺血性损伤的动物产生更严重的31P MRS能量衰竭。此外,每隔1小时缺血发作的重复导致每次缺血发作后自发性皮层电抑制持续时间的逐渐延长。然而,缺血前缺氧(5% O2 5分钟)导致MRS测量中磷酸肌酸和细胞内无机磷酸盐水平的微小变化,否则脑电图活动逐渐下降。脑电图的这种关闭反应可以被推断为保存大脑的能量状态,尽管它不能阻止脑缺血后水肿和神经元死亡的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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