低温对脑缺血-再灌注大鼠α-酮戊二酸脱氢酶复合物活性及脑梗死体积的影响

目的观察不同温度下脑缺血-再灌注大鼠线粒体α-酮戊二酸脱氢酶复合物（α—KGDHC）活性及脑梗死体积的变化，进一步探讨不同低温的神经保护机制。方法取雄性SD大鼠35只，按随机数字法分为假手术组（n=5）及大脑中动脉闭塞2h再灌注组（n=30），后者根据再灌注时温度的不同，再分为37℃、33℃及28℃组（n=10）。采用线栓法制备脑缺血-再灌注大鼠模型，再灌注时利用降温毯降温，使肛温分别保持37℃、33℃及28℃，时间为3h。在缺血后24h时检测各组大鼠双侧大脑皮质和海马区线粒体α—KGDHC活性及脑梗死体积。结果①假手术组、37℃组、33℃组、28℃组缺血侧皮质α-KGDHC分别为（20．1±1．3）、（9．5±0．9）、（15．2±1．1）、（5．5±1．2）mU／mg（蛋白）；海马区为（17．1±1．1）、（8．1±1．1）、（12．2±1．0）、（4．1±1．1）mU／mg（蛋白）。33℃组与37℃组和28℃组比较，差异均有统计学意义（P〈0．01）。②37℃组脑梗死的体积最大，占对侧大脑半球的（48．2±1．1）％，33℃组梗死体积最小，占（31．6±1．3）％，28℃组占（34．8±1．2）％，三组比较差异有统计学意义（P〈0．01）。结论提高缺血-再灌注大鼠线粒体α-KGDHC活性是低温干预的神经保护作用机制之一。33℃低温比28℃低温有更好的效果。

Effect of different hypothermia on mitochondrial alpha-ketoglutarate dehydrogenase complex and cerebral infarction volume in focal cerebral ischemia-reperfusion in rats

Objective To observe the activity of mitochondrial alpha-ketoglutarate dehydrogenase complex （KGDHC） and the changes of volume of cerebral infarction under the different hypothermia interventions in focal cerebral ischemia-reperfusion in rats and to further study the neuroprotective mechanisms of different hypothermia. Methods Thirty-five male Sprague-Dawley rats were randomly allocated into sham-operation group （ n = 5 ） and reperfusion 2 hours after middle cerebral artery occlusion （ n = 30 ） group. The latter were redivided into 37℃ , 33℃ and 28℃ groups （ n = 10 in each group） according to different hypothermia. The bilateral cerebral cortices, the activity of mitochondrial KGDHC in hippocampal region and the volume of cerebral infarction were detected at 24 hours after ischemia. Results The KGDHC in the cortex of ischemic side at 24 hours after ischemia in the sham-operation, 37℃, 33℃, and 28℃ groups were 20.1 ± 1.3, 9.5 ± 0. 9, 15.2 ± 1.1, and 5.5 ± 1.2 mU/mg protein, respectively; in the hippocampal area they were 17.1 ± 1.1, 8. 1 ± 1.1, 12. 2 ± 1.0, and 4. 1± 1.1 mU/mg protein, respectively. There were significant differences between the 33℃ group and the 37℃ and 28℃ groups （P 〈0. 01 ）. The volume of cerebral infarction was the largest in the 37℃ group, and it accounted for 48.2 ± 1.1% of the contralateral hemisphere; the volume of cerebral infarction was the smallest in the 33℃ group, and it accounted for 31.6 ± 1.3% of the contralateral hemisphere; and it accounted for 34.8±1.2% in the 28℃ group. There were significant differences among the 3 groups （ P 〈 0. 01 ）. Conclusion Increasing the activity of mitochondrial KGDHC in focal cerebral ischemia-reperfusion in rats is one of the neuroprotective mechanisms of hypothermic intervention. Hypothermia at 33℃ has better effect than that at 28℃.