Neuroprotective consequences of postconditioning on embolic model of cerebral ischemia in rat

It has been reported that ischemic postconditioning, conducted by a series of brief occlusion and release of the bilateral common carotid arteries, confers neuroprotection in permanent or transient models of stroke. However, consequences of postconditioning on embolic stroke have not yet been investigated.

In the present study, rats were subjected to embolic stroke (n=30) or sham stroke (n=5). Stroke animals were divided into control (n=10) or three different patterns of postconditioning treatments (n=20). In the first pattern of postconditioning (PC10, n=10), the common carotid arteries (CCA) were occluded and reopened 10 and 30 sec, respectively for 5 cycles. Both occluding and releasing times in pattern 2 (PC30, n=5) and 3 (PC60, N=5) of postconditionings, were five cycles of 30 or 60 sec, respectively. Postconditioning was induced at 30 min following the stroke. Subsequently, cerebral blood flow (CBF) was measured from 5 min before to 60 min following to stroke induction. Infarct size, brain edema and neurological deficits and reactive oxygen species (ROS) level was measured two days later.

While PC10 (P<0.001), PC30 and PC60 (P<0.05) significantly decreased infarct volume, only PC10 decreased brain edema and neurological deficits (P<0.05). Correspondingly, PC10 prevented the hyperemia of brain at 35, 40, 50 and 60 min after the embolic stroke (P<0.005). No significant difference in ROS level was observed between PC10 and control group.

Ischemic postconditioning reduces infarct volume and brain edema, decreases hyperemia following to injury and improves neurological functions after the embolic model of stroke.