Bradykinin postconditioning ameliorates focal cerebral ischemia in the rat

• We tested possible delay of postconditioning after MCAO.
• Regional distribution of SOD changes after ischemia was followed.
• We confirmed that bradykinin is effective postconditioner also after transient focal ischemia.

The goal of this study is to investigate the effects of bradykinin (BR) postconditioning on cerebral ischemic injury. Transient focal cerebral ischemia was induced in rats by 60 min of middle cerebral artery occlusion (MCAO), followed by 3 days of reperfusion. BR as a postconditioner at a dose of 150 μg/kg was applied intraperitoneally 3, 6, 24 and 48 h after MCAO. BR postconditioning significantly reduced total infarct volumes if applied 3 h after MCAO by 95%, 6 h after MCAO by 80% and 24 h after MCAO by 70% in versus vehicle group. Neurological functions were a marked improvement in the BR groups compared to the ischemia group. The number of degenerated neurons in the hippocampal CA1 region was also significantly lower in BR-treated ischemic groups compared to vehicle group. BR postconditioning prevented the release of MnSOD from the mitochondria and reduced the activity of the total SOD and CAT if it is administrated short time after stroke. Our data proves the ischemic tolerance in the brain induced by BR postconditioning resulted as effective agent against as strong an attack as 60 min MCAO even when used many hours after ischemia.