Chen H, Chopp M, Zhang Z G, Garcia J H
Department of Neurology, Henry Ford Hospital, Detroit, Michigan 48202.
J Cereb Blood Flow Metab. 1992 Jul;12(4):621-8. doi: 10.1038/jcbfm.1992.86.
We investigated the effect of moderate whole body hypothermia (30 degrees C) on transient middle cerebral artery occlusion (MCAO) in the rat. Male Wistar rats were subjected to 2 h of ischemia by inserting a suture into the lumen of the internal carotid artery and occluding the origin of the MCA. Experimental groups were (a) MCAO induced at 37 degrees C body temperature (n = 15); (b) 30 degrees C body temperature induced prior to ischemia and maintained for 2 h of MCAO and 1 h of reperfusion (n = 12); and (c) MCAO with regional brain and body temperatures measured in normothermic (n = 3) and hypothermic MCAO rats (n = 2). Histopathological evaluation was performed 96 h after reperfusion. All normothermic MCAO animals exhibited ischemic infarct involving the ipsilateral cortex and basal ganglia with infiltration of neutrophils, macrophages, and microvascular proliferation. Hypothermic MCAO animals exhibited minor ischemic damage ranging from selective neuronal injury to small focal areas of infarct with minimal inflammatory response. Our data demonstrate that transient ischemia induced by using the intra-arterial suture method to occlude the MCA results in a reproducible brain lesion and that moderate hypothermia has a profound protective effect on the brain injury after transient MCAO.
我们研究了中度全身低温(30摄氏度)对大鼠短暂性大脑中动脉闭塞(MCAO)的影响。通过将缝线插入颈内动脉管腔并阻塞大脑中动脉起始部,使雄性Wistar大鼠经历2小时的缺血。实验组包括:(a)体温37摄氏度时诱导MCAO(n = 15);(b)缺血前诱导至30摄氏度体温,并在MCAO 2小时和再灌注1小时期间维持该体温(n = 12);以及(c)测量正常体温(n = 3)和低温MCAO大鼠(n = 2)的局部脑和体温的MCAO。再灌注96小时后进行组织病理学评估。所有正常体温的MCAO动物均表现出涉及同侧皮质和基底神经节的缺血性梗死,伴有中性粒细胞浸润、巨噬细胞浸润和微血管增殖。低温MCAO动物表现出轻微的缺血性损伤,范围从选择性神经元损伤到小的局灶性梗死区域,炎症反应最小。我们的数据表明,使用动脉内缝线法阻塞大脑中动脉诱导的短暂性缺血会导致可重复的脑损伤,并且中度低温对短暂性MCAO后的脑损伤具有深远的保护作用。