Ischemia-induced development of cerebral edema in awake and anesthetized gerbils.

N L Edgehouse, R V Dorman
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引用次数: 9

Abstract

General anesthesia is often used to immobilize experimental animals prior to the induction of cerebral ischemia. However, anesthetics are known to alter many of the biochemical and physiological parameters used for the assessment of stroke-induced brain damage. We examined the effects of bilateral carotid artery ligations on mortality and the development of cerebral edema in unanesthetized gerbils. We found that increasing the length of the ischemic episode resulted in increased mortality, both during the ischemic period and during cerebral reperfusion. The duration of the ischemic episode was also correlated with the rate and degree of the development of cerebral edema. Both of these estimates of ischemia-induced brain damage were significantly reduced by the pretreatment of the animals with pentobarbital. Based on the variable effects of different anesthetics on CNS activities, and the observed effects of barbiturate anesthesia on ischemia-induced mortality and edema development in the present model, we suggest that it may be inappropriate to anesthetize experimental animals when investigating certain aspects of stroke-induced brain damage.

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清醒和麻醉沙鼠脑水肿的缺血诱导发展。
在脑缺血诱导前,全身麻醉常用于固定实验动物。然而,已知麻醉剂会改变许多用于评估中风引起的脑损伤的生化和生理参数。我们研究了双侧颈动脉结扎对未麻醉沙鼠死亡率和脑水肿发展的影响。我们发现,缺血发作时间的增加导致缺血期和脑再灌注期间死亡率的增加。缺血发作的持续时间也与脑水肿的发展速度和程度相关。这两种缺血性脑损伤的估计都被戊巴比妥预处理的动物显著降低。基于不同麻醉药对中枢神经系统活动的不同影响,以及在本模型中观察到的巴比妥酸盐麻醉对缺血致死亡和水肿发展的影响,我们认为在研究中风致脑损伤的某些方面时,麻醉实验动物可能是不合适的。
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The mechanism of ischemia-induced brain cell injury. The membrane theory. Peroxidative damage to cell membranes following cerebral ischemia. A cause of ischemic brain injury? Phosphoinositide turnover and calcium ion mobilization in receptor activation. Polyamines in cerebral ischemia. Reduction of neural damage in irreversible cerebral ischemia by calcium antagonists.
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