Ridenour T R, Warner D S, Todd M M, McAllister A C
Department of Surgery, University of Iowa, Iowa City 52242.
Stroke. 1992 May;23(5):733-8. doi: 10.1161/01.str.23.5.733.
Mild hypothermia (32-35 degrees C) has been repeatedly shown in laboratory models to reduce damage resulting from global cerebral ischemic insults. Little information is available, however, regarding the protective potential of mild hypothermia against focal ischemia. We designed the present study to determine whether mild hypothermia influences outcome from either temporary or permanent middle cerebral artery occlusion in the rat.
In experiment 1 (permanent occlusion), mechanically ventilated, halothane-anesthetized spontaneously hypertensive rats underwent permanent ligation of the middle cerebral artery. Pericranial temperature was maintained at either 37 degrees C (n = 11) or 33 degrees C (n = 11) during the first 2 hours of occlusion. In experiment 2 (temporary occlusion), the vessel was occluded for 1 hour only. Pericranial temperature was controlled at either 37 degrees C (n = 12) or 33 degrees C (n = 14) during ischemia and for 1 hour after reperfusion. In both experiments, the rats were allowed to recover, with neurological function scored at 24 and 96 hours after onset of ischemia. Cerebral infarct volume (as determined by nitro blue tetrazolium staining) was planimetrically evaluated 96 hours after onset of ischemia.
No difference in infarct volume was observed between groups undergoing permanent occlusion (177 +/- 53 mm3 for 37 degrees C rats, 167 +/- 71 mm3 for 33 degrees C rats [mean +/- SD]). Although neurologic function correlated with infarct volume at 96 hours (all animals in experiment 1 combined; p less than 0.01), we were unable to demonstrate an intergroup difference in function. In animals undergoing temporary occlusion, mean +/- SD infarct volume was 48% less in the hypothermic group (89 +/- 54 mm3 for 37 degrees C, 46 +/- 31 mm3 for 33 degrees C; p less than 0.03). Neurological function again correlated with infarct size (p less than 0.02), but improvement in function approached significance for the hypothermic group (p less than 0.06) at 24 hours after reperfusion only.
Benefits from mild hypothermia may be obtained under conditions of temporary but not permanent middle cerebral artery occlusion in the rat.
在实验室模型中，多次证明轻度低温（32 - 35摄氏度）可减轻全脑缺血性损伤所导致的损害。然而，关于轻度低温对局灶性缺血的保护潜力，目前所知甚少。我们设计了本研究，以确定轻度低温是否会影响大鼠大脑中动脉临时或永久性闭塞后的结果。
在实验1（永久性闭塞）中，对机械通气、氟烷麻醉的自发性高血压大鼠进行大脑中动脉永久性结扎。在闭塞的前2小时内，颅周温度维持在37摄氏度（n = 11）或33摄氏度（n = 11）。在实验2（临时闭塞）中，血管仅闭塞1小时。在缺血期间及再灌注后1小时，颅周温度控制在37摄氏度（n = 12）或33摄氏度（n = 14）。在两个实验中，均让大鼠恢复，并在缺血发作后24小时和96小时对神经功能进行评分。在缺血发作后96小时，通过硝基蓝四氮唑染色测定脑梗死体积，并进行平面测量评估。
在永久性闭塞组之间，未观察到梗死体积有差异（37摄氏度组大鼠为177±53立方毫米，33摄氏度组大鼠为167±71立方毫米[均值±标准差]）。虽然在96小时时神经功能与梗死体积相关（实验1中的所有动物合并；p < 0.01），但我们未能证明两组之间在功能上存在差异。在进行临时闭塞的动物中，低温组的平均梗死体积±标准差减少了48%（37摄氏度组为89±54立方毫米，33摄氏度组为46±31立方毫米；p < 0.03）。神经功能再次与梗死大小相关（p < 0.02），但仅在再灌注后24小时，低温组的功能改善接近显著水平（p < 0.06）。
在大鼠大脑中动脉临时而非永久性闭塞的情况下，可能会从轻度低温中获益。
