Karibe H, Zarow G J, Weinstein P R
Department of Neurological Surgery, School of Medicine, University of California, San Francisco, USA.
J Neurosurg. 1995 Jul;83(1):93-8. doi: 10.3171/jns.1995.83.1.0093.
To determine which of two treatments for reducing ischemic injury after temporal focal ischemia is more effective, the effects of mild (33 degrees C) intraischemic hypothermia were compared with those of mannitol, the most commonly used neuroprotective agent. Four groups of Sprague-Dawley rats underwent 1 hour of endovascular middle cerebral artery occlusion followed by 23 hours of normothermic reperfusion. The four experimental groups were as follows: Group A, saline control; Group B, mannitol (25%, 1 g/kg); Group C, hypothermia; and Group D, hypothermia plus man-nitol. Laser-Doppler estimates of cortical blood flow showed that hypothermia did not affect blood flow during ischemia or reperfusion. Mannitol increased cortical blood flow during ischemia and reperfusion under both normothermic and hypothermic conditions (p < 0.05). Neurological deficit was significantly less severe in treated rats (Group B, p < 0.05; Group C or D, p < 0.01) than in controls (Group A). Infarct volume, measured on semiserial Nissl-stained sections, was significantly smaller in treated rats (p < 0.01) than in controls. Infarct volume was also significantly smaller in rats treated with hypothermia than in those treated with mannitol (Group C vs. Group B, p < 0.05); there was no difference between rats treated with mannitol and those treated with mannitol and hypothermia. All three treatments reduced infarct area in the ischemic penumbra; hypothermia with or without mannitol also reduced infarct area in the ischemic core. These results demonstrate that both mild intraischemic hypothermia and mannitol reduce infarct size and neurological deficit: hypothermia reduces infarct size more effectively than mannitol, and mannitol adds no significant protection to hypothermia, whereas hypothermia adds significant protection beyond that afforded by mannitol after brief focal ischemia followed by reperfusion in rats. The results suggest that mild intraischemic hypothermia alone, or in combination with mannitol, may be useful in avoiding ischemic injury from temporary vessel occlusion during cerebrovascular surgery.
为了确定两种减轻颞叶局灶性缺血后缺血性损伤的治疗方法中哪种更有效，将轻度（33摄氏度）缺血期低温疗法的效果与最常用的神经保护剂甘露醇的效果进行了比较。四组斯普拉格-道利大鼠接受1小时的血管内大脑中动脉闭塞，随后进行23小时的常温再灌注。四个实验组如下：A组，生理盐水对照；B组，甘露醇（25%，1克/千克）；C组，低温疗法；D组，低温疗法加甘露醇。激光多普勒对皮质血流的估计显示，低温疗法在缺血期或再灌注期不影响血流。在常温和低温条件下，甘露醇在缺血期和再灌注期均增加皮质血流（p<0.05）。治疗组大鼠（B组，p<0.05；C组或D组，p<0.01）的神经功能缺损明显轻于对照组（A组）。在半连续尼氏染色切片上测量的梗死体积，治疗组大鼠明显小于对照组（p<0.01）。低温治疗的大鼠梗死体积也明显小于甘露醇治疗的大鼠（C组与B组，p<0.05）；甘露醇治疗的大鼠与甘露醇加低温治疗的大鼠之间无差异。所有三种治疗方法均减少了缺血半暗带的梗死面积；有或没有甘露醇的低温疗法也减少了缺血核心区的梗死面积。这些结果表明，轻度缺血期低温疗法和甘露醇均能减少梗死体积和神经功能缺损：低温疗法比甘露醇更有效地减少梗死体积，甘露醇对低温疗法无显著的额外保护作用，而在大鼠短暂局灶性缺血后再灌注，低温疗法比甘露醇提供了显著的额外保护。结果表明，单独的轻度缺血期低温疗法或与甘露醇联合使用，可能有助于避免脑血管手术中临时血管闭塞引起的缺血性损伤。
