Neuroprotective effects of the hypothermia on permanent and transient cerebral ischemia

脑低温是否被确立为永久性局灶性脑缺血的临床治疗工具还有待进一步研究。第一项研究旨在比较选择性脑低温6h对左侧大脑中动脉闭塞后6(实验1-1)、24(实验L-2)、48(实验1-3)和168(实验1-4)h的中风动物最终结局的影响。均经气管插管、人工呼吸。将大脑中动脉(MCAO)近端电凝后切断，采用自行设计的表面线圈加冰水灌流的方法，在全麻下即刻开始选择性脑低温(SBH)(A组)。在受…组影响的动物中S B、C较多，麻醉期间脑温保持正常。实验期间连续记录脑温、直肠温度、血压和血气。每只动物在复温后拔管，在室温下饲养在养殖笼中，直到被杀。在实验结束时，对大脑进行经心脏灌流并取出。在第二个实验中，我们改进了我们的方法，提供了一种侵入性较小的方法。两种方法的不同之处在于面罩麻醉和自主呼吸，改良的方法只需在MCAO后即刻进行4h的脑低温。比较假手术组、假手术组和假手术组大鼠脑缺血后168h的脑温度变化，结果显示，脑缺血后20min，脑温度即达32℃，此后一直维持在30min左右。完全重新升温只需要一个小时。全身各参数均未见异常。脑梗塞体积(mm~3平均±标准差)如下。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。经方差分析，本型SBH可显著缩小脑缺血后168小时的脑梗塞体积。本研究结果为脑卒中的治疗开辟了一条新的途径。较少

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