Neuroprotective effects of the hypothermia on permanent and transient cerebral ischemia

脑低温治疗能否作为永久性局灶性脑缺血的临床治疗手段仍有待进一步研究。第一项研究旨在比较6小时选择性脑低温对实验抚摸动物最终结果的影响。阻断左大脑中动脉后分别死亡6（实验1-1）、24（实验1- 2）、48（实验1-3）和168（实验1-4）小时。将116只Sprague-Dawley大鼠分为上述4组，每组包括对照组（B组）和假手术组（C组）。经气管插管，人工通气。电凝大脑中动脉（MCAo）近端，然后切开。我们最初的表面线圈灌注冰水的方法使我们能够在全身麻醉（a组）下6小时的MCAo后立即开始选择性脑低温（SBH）。B、C组大鼠麻醉期间脑温保持正常。实验过程中，连续记录脑温、直肠温、血压和血气。每只动物复温后拔管，置于室温培养笼中饲养至处死。在实验结束时，经心脏灌注大脑并将其移除。脑切片染色以测量梗死体积。在第二个实验中，我们对方法进行了改进，提供了侵入性较小的方法。两种方法的不同之处在于，改进后的方法在MCAo后立即保持面罩麻醉和自主呼吸，仅进行4小时的脑低温。比较SBH组、对照组和假手术组对MCAo 168小时梗死面积的影响。SBH组脑温在MCAo后20分钟内达到32℃，在SBH期间保持在30℃左右。完全恢复体温只需要一个小时。系统参数未见异常。梗死体积（mm3平均值±标准差）如下：实验1-1 (n=27) A (n=16)60±28,B (n=8) 130±6,C (n=3) 11±2；实验1-2 (n=25) A (n=14) 84±25,B (n=6) 137±27,C (n=5) 4±4；实验1-3 (n=21) A (n=8) 33±11,B (n=8) 96±25，C(n=5) 7±7；实验1 - 4 (n = 10) (n = 5) 41±20,86±23 B (n = 3), C (n = 2) 6±7;实验2 (n=33) A (n=11) 25±18,B (n=13) 100±41,C (n=9) 2±2本型SBH在缺血后168 h内均能显著减小梗死体积，方差分析p值均小于0.05。目前的结果为脑中风开辟了一种新的有希望的治疗策略。少

Whether brain hypothermia is established as a tool for the clinical treatment of the permanent focal cerebral isehemia remains to be yet. The first study aimed at comparing the effects of the 6 hour of selective brain hypothermia on final outcome of the experimental stroked animals.which were killed 6 (Experiment 1-1), 24 (Experiment l-2), 48 (Experiment 1-3) and 168 (Experiment 1-4) hours after occlusion ofleft middle cerebral artery.A total of 116 Sprague-Dawley rats were divided into the above 4 groups, each of which included control animals (Group B)and sham-operated ones (Group C). They were endotracheally intubated and ventilated artificially. The proximal portion of the middle cerebral artery (MCAo) was electrically coagulated and then cut.Our original methodology of the surface coil which perfused ice water enabled us to start selective brain hypothermia (SBH) immediately after MCAo during a period of 6 hours under general anesthesia (Group A). In the animals subjected to Group … More s B and C, the brain temperature was kept normal during the anesthesia. During the experiment, the brain temperature, the rectal temperature, blood pressure and blood gas were continually recorded. Each animal was extubated after the rewarming, and bred in the cultivating cage at room temperature until they were killed. At the end of experiments, the brain was perfused transcardially and removed. The brain slices were stained for measuring an infarction volume.In the second experiment, our methodology was refined on, providing the less invasive method. The difference between these two methods is to keep anesthesia by mask and spontaneous respiration and only 4 hour of brain hypothermia immediately after MCAo in the refined one. The effects of SBH on infarct size at 168 hours of MCAo were compared among the SBH-, control and sham-operated groups.The brain temperature of the SBH-group reached 32℃ within 20 minutes after the MCAo, and then stayed around 30 during the SBH. A complete rewarming needed only one hour. No abnormal finding was demonstrated in the systemic parameters. The infarction volume (mm3 mean ± standard deviation) was as follows. Experiment 1-1 (n=27) A (n=16)60 ±28, B (n=8) 130±6, C (n=3) 11±2; Experiment 1-2 (n=25) A (n=14) 84±25, B (n=6) 137±27, C (n=5) 4 ± 4; Experiment 1-3 (n=21) A (n=8) 33±11, B (n=8) 96±25, C(n=5) 7±7; Experiment 1-4 (n=l0) A (n=5) 41±20, B(n=3) 86±23, C(n=2) 6±7; Experiment 2 (n=33) A (n=11) 25±18, B (n=13) 100±41, C (n=9) 2±2The present type of SBH is shown to significantly reduce the infarction volume up to 168 hours after the onset of ischemia, from the analysis of variance with the p-value of less than 0.05. The present results open up a new promising therapeutic strategy against the brain stroke. Less