M Mobini - Master of Physiology, Physiology-Pharmacology Research Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
H Rezazadeh - Master of Physiology, Physiology-Pharmacology Research Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
A Shamsizadeh - Associate Professor of Physiology, Physiology-PharmacologyResearch Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
V Ehsani - Master of Physiology, Physiology-Pharmacology Research Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
E Hakimizadeh - Master of Physiology, Physiology-Pharmacology Research Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
S Amir-Esmaili - Master of Physiology, Physiology-Pharmacology Research Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran
M Allahtavakoli - Associate Professor of Physiology, Physiology-PharmacologyResearch Center, Rafsanjan University ofMedical Sciences, Rafsanjan, Iran

Background & Aims: Ischemic postconditioning, conducted by a series of brief occlusion and release of the bilateral common carotid arteries, has neuroprotective properties in permanent or transient models of middle cerebral artery (MCA) occlusion but its delayed neuroprotective effects in the embolic model of stroke, especially in female rat, have not yet been reported and were investigated in the current study. Methods: In this experimental study, ۲۴ female Wistar rats (۲۰۰ to ۲۵۰ g) were divided into three groups of sham, stroke and postconditioning. All animals were similar in reproductive cycle, and after that, stroke was induced by clot injection into the right middle cerebral artery. For postconditioning, common carotid arteries (CCA) were occluded for ۳۰ seconds and reopened for ۳۰ seconds, for ۵ cycles. The postconditioning was induced at ۶.۵ hours after the stroke. Infarction volume, brain edema and neurological deficits were measured two days later. Results: Postconditioning at ۶.۵ hours after stroke decreased infarction volume (P< ۰.۰۰۱), brain edema (P<۰.۰۵۰) and norologic deficit (P<۰.۰۵۰) significantly compared to the stroke group. Conclusion: Late postconditioning improved ischemic injury, brain edema and neurological functions after the embolic model ofstroke in female rat.

Brain ischemia, Ischemic postconditioning, Reperfusion, infarction, Neurological disorders