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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Transient cooling during early reperfusion attenuates delayed edema and infarct progression in the Spontaneously Hypertensive Rat. Distribution and time course of regional brain temperature change in a model of postischemic hypothermic protection.
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Transient cooling during early reperfusion attenuates delayed edema and infarct progression in the Spontaneously Hypertensive Rat. Distribution and time course of regional brain temperature change in a model of postischemic hypothermic protection.

机译:早期再灌注期间的短暂降温可减轻自发性高血压大鼠的延迟性水肿和梗塞进展。局部缺血后低温保护模型中区域脑温度变化的分布和时程。

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The temperature threshold for protection by brief postischemic cooling was evaluated in a model of transient focal ischemia in the Spontaneously Hypertensive Rat, using an array of epidural probes to monitor regional brain temperatures. Rats were subjected to 90 mins tandem occlusion of the right middle cerebral artery (MCA) and common carotid artery. Systemic cooling to 32 degrees C was initiated 5 mins before recirculation, with simultaneous brain cooling to temperatures ranging from 28 degrees C to 32 degrees C within the MCA territory by means of a temperature-controlled saline drip. Rewarming was initiated at 2 h recirculation and was complete within 30 mins. Tissue damage and edema volume showed clear temperature-dependent reductions when evaluated at 3 days survival, with no protection evident in the group at 32 degrees C but progressive effects on both parameters after deeper cooling. A particularly striking effect was the essentially complete elimination of edema progression between 1 and 3 days. Temperature at distal sites within the MCA territory better predicted reductions in lesion volume, indicating that protection required effective cooling of the penumbral regions destined to be spared. These results show that even brief cooling can be highly protective when initiated at the time of recirculation after focal ischemia, but indicate a substantially lower temperature threshold for hypothermic protection than has been reported for other strains, occlusion methods, and cooling durations.
机译:使用一系列硬膜外探针监测局部脑温度,在自发性高血压大鼠的短暂局灶性局部缺血模型中评估了短暂缺血后冷却保护的温度阈值。大鼠右脑中动脉(MCA)和颈总动脉串联90分钟。在再循环前5分钟开始将全身冷却至32摄氏度,同时通过温度控制的盐水滴注将大脑同时冷却至MCA区域内的28摄氏度至32摄氏度。在2小时的再循环中开始重新加热,并在30分钟内完成。在3天生存时进行评估时,组织损伤和水肿体积显示出明显的温度依赖性降低,在32°C的组中没有明显的保护作用,但是在深冷后对这两个参数的影响逐渐增加。一个特别显着的效果是在1至3天之间基本上完全消除了水肿。 MCA区域内远端部位的温度更好地预测了病变体积的减少,这表明保护需要有效冷却注定要幸免的半影区。这些结果表明,在局灶性缺血后的再循环时,即使短暂的降温也可以起到高度保护作用,但与其他菌株,闭塞方法和冷却时间相比,低温保护的温度阈值要低得多。

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