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

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.