缺血后适应对大鼠脑缺血/再灌注损伤的影响

Effects of ischemic postconditioning on cerebral ischemia/reperfusion injury in rats

目的:探讨缺血后适应对大鼠脑缺血/再灌注损伤的影响。方法:应用线栓法制作大鼠脑缺血/再灌注损伤模型;21只雄性SD大鼠随机分为缺血/再灌注组、夹闭单侧颈总动脉后处理组和夹闭双侧颈总动脉后处理组,每组7只。再灌注48h,测定脑梗死体积;拔栓后1h及处死大鼠前进行神经功能测定;梗死即刻、梗死后10min、术中1h、拔栓后即刻、每次夹/松颈总动脉时、干预后30min等15个时点监测脑血流。结果:夹闭单侧、双侧颈总动脉后处理组大鼠脑组织梗死体积与缺血/再灌注组相比明显减小,有显著差异;3组脑血流各个时点方差分析差异无显著,但是夹闭双侧颈总动脉后处理组干预30min后脑血流百分比较缺血/再灌注组、夹闭单侧颈总动脉后处理组降低9%。手术后1h3组神经功能评分P<0.05,差异显著,夹闭单侧、双侧颈总动脉后处理组神经功能缺损均比缺血/再灌注组减轻。结论:缺血后适应能够明显减小梗塞体积,改善大鼠术后1h神经功能评分,可能与缺血后适应调节早期再灌注时血流动力学状态有关。

AIM ： To study the effects of ischemic postconditioning on cerebral ischemia following middle cerebral artery occlusion in rats. METHODS： 21 rats were randomly divided into three groups： middle cerebral artery occlusion （ MCAO）, MCAO ＋ transient unilateral common carotid artery occlusion （ u - CCA - O）, MCAO ＋ transient bilateral common carotid artery occlusion （ b - CCA - O） （ n = 7, respectively）, u - CCA - O/b - CCA - O was generated by transient middle cerebral artery occlusion plus transient unilateral/bilateral common carotid artery （CCA） occlusion. After the suture was removed, ischemic postconditioning was performed by occluding CCA for 10s, reperfusion 10s, and then allowing for another 4 cycles of 10s of reperfusion and 10s of CCA occlusion. Rats were sacrificed 2 d later and infarct size was measured. Cerebral blood flow （CBF） was measured in different 15 time points： 0 min, 10 min, 1 h after MCA occlusion, 0 min after MCA reperfusion, 10s of CCA occlusion and 10s of CCA reperfusion in all five cycles, 30 min after MCA reperfusion. Functional neurological outcome was determined 1 h and 48 h after reperfusion. Infarct volume was measured 48 h after reperfusion. RESULTS ： The infarct volumes in u - CCA - O group and b - CCA - O group diminished compared to the control group. The results of CBF demonstrated that b - CCA - O group diminished 9% compared with control and u - CCA - O group when 30 min after intervention. The rats in u - CCA - O and b - CCA - O group had better neurological performance at 1 h after reperfusion. CONCLUSION： Ischemic postconditioning reduces infarct size, improves functional neurological outcome, most plausibly by diminishing cerebral blood flow.