Canevari L, Console A, Tendi E A, Clark J B, Bates T E
Department of Neurochemistry, Institute of Neurology, Queen Square, London WC1N 3BG,
Brain Res. 1999 Jan 30;817(1-2):241-5. doi: 10.1016/s0006-8993(98)01278-5.
In order to test the effect of hypothermia on mitochondrial function damage following cerebral ischaemia/reperfusion, Mongolian gerbils were submitted to 30 min bilateral carotid occlusion and 2 h of reperfusion at 37 degreesC or 30 degreesC. After normothermic (37 degreesC) ischaemia/reperfusion, significant decreases in mitochondrial state 3 (+ADP) oxygen consumption (-42.2%), complex II-III activity in synaptosomes (-31.7%) and complex IV were measured, in both free mitochondria and synaptosomes (-30.3% and -27. 8% respectively). However, following hypothermic (30 degreesC) reperfusion, both respiration rates and all enzyme activities remained at levels not significantly different from those in the sham operated controls.
为了测试低温对脑缺血/再灌注后线粒体功能损伤的影响，将蒙古沙鼠进行30分钟的双侧颈动脉闭塞，并在37℃或30℃下再灌注2小时。在常温（37℃）缺血/再灌注后，测量到线粒体状态3（+ADP）氧消耗显著降低（-42.2%），突触体中复合物II-III活性降低（-31.7%），游离线粒体和突触体中的复合物IV也降低（分别为-30.3%和-27.8%）。然而，在低温（30℃）再灌注后，呼吸速率和所有酶活性均保持在与假手术对照组无显著差异的水平。
