Abstract TP259: Ischemic Postconditioning Protects Against Focal Ischemia in Mouse
Ischemic Postconditioning Protects Against Focal Ischemia in Mouse
Background: Ischemic postconditioning(IPost) has been shown to attenuate cerebral ischemia/reperfusion injury in a few rat models. Here we further established a IPost model in mice, which offers oppotunities to study protective mechanism of IPost in mice with various genetic backgrounds.
Material and Methods: Focal ischemia was induced by middle cerebral artery (MCA) suture occlusion for 45min. IPost was conducted by a series of repetitive, brief occlusion/reperfusion via withdrawl and insertion of the suture in the internal carotid artery. Infarction sizes were measured 3 days or 2 weeks after stroke. Functional neurological scores were also assessed.
Results: we found that rapid IPost with three cycles of occlusion/reperfusion (15sec/30sec), or with two cycles of occlusion/reperfusion ( 60sec/60sec), which were performed 2 min after reperfusion, significantly reduced infarct sizes as measured 3 days post-stroke. Delayed IPost performed 3 hours after reperfusion aslo significantly reduced infarct sizes( n=9, P<0.01). Rapid IPost with 3 cycles of occlusion/reperfusion(15/30s) initiated 2 min after reperfusion resulted in the smallest infarct size. The spared infarct area were seen in border zones between the cortical territories of the anterior cerebral artery(ACA) and those of the MCA, as well as in the ventromedial and dorsolateral striatum. Delayed brain injury measured by silver staining 2 weeks after stroke and mortality were also reduced by rapid IPost.
Conclusions: IPost reduces cerebral infarction and improve functional neurological status in mice, which offers a model to investigate the underlying protective mechanism of postconditioning using mice with various genetic backgrounds in the future.
- © 2012 by American Heart Association, Inc.