Neuroprotective effects of the hypothermia on permanent and transient cerebral ischemia

脑低温是否能作为临床治疗永久性局灶性脑缺血的一种手段，目前尚不清楚。第一项研究旨在比较6小时选择性脑低温对实验性中风动物最终结局的影响。（实验1-1），24（实验1 -2），48（实验1-3）和168（实验1-4）将116只SD大鼠随机分为4组，每组包括对照组（B组）和假手术组（C组）。对他们进行了气管内插管和人工通气。采用电凝大脑中动脉（MCAo）近端，然后切断MCAo，在全身麻醉（A组）下，采用表面线圈灌注冰水的方法，使我们能够在MCAo后立即开始选择性脑低温（SBH），持续6小时。在组动物中， ...更多信息 s B和C，在麻醉期间保持脑温正常。在实验过程中，连续记录脑温、肛温、血压和血气。复温后拔管，室温饲养至处死。在实验结束时，经心脏灌注大脑并取出。在第二个实验中，我们改进了我们的方法，提供了一种创伤性较小的方法。两种方法的不同之处在于改良法采用面罩和自主呼吸维持麻醉，而改良法仅在MCAo后即刻进行4 h的脑低温。SBH组脑温在MCAo后20分钟内达32℃，SBH期间维持在30 ℃左右。完全复温只需要一个小时。系统参数未显示异常结果。梗死体积（mm 3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）A（n=5）41±20，B（n=3）86±23，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本类型的SBH显示在缺血发作后168小时显著减少梗塞体积，根据方差分析，p值小于0.05。目前的结果开辟了一个新的有前途的治疗策略，对脑卒中。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