This study explores the development of a rat model for cerebral ischemia-reperfusion injury and evaluates the effects of varying reperfusion durations on the severity and progression of the injury. The findings aim to provide a scientific model for the advancement of more effective prevention and treatment strategies. Male Sprague-Dawley rats, each weighing approximately 260 grams, were utilized as experimental subjects. Following a one-week acclimatization period, surgical procedures were conducted. The middle cerebral artery was occluded using a suture for 90 minutes, followed by reperfusion. Brain tissue samples were collected at 1, 7, and 14 days post-reperfusion.We monitored the body weight of rats and employed the Neurological Deficit Score to assess behavioral changes across different groups. Hematoxylin and eosin (HE) staining was utilized to examine pathological damage in brain tissue at various time points, providing clear visualization of brain cell morphology. The 2,3,5-triphenyltetrazolium chloride (TTC) staining method was used to evaluate cerebral infarction volumes at different time intervals. The rats exhibited different body weight changes and neurological deficits at different time points. The volume of cerebral infarction and the extent of pathological damage in rat brain tissue exhibited significant variation across different time points. HE staining demonstrated nuclear condensation, fragmentation, and dissolution in rat brain tissue at one day post-reperfusion. By seven days post-reperfusion, irregular cellular arrangement persisted, accompanied by extensive vacuolar edema and degeneration. At fourteen days post-reperfusion, vacuolar edema decreased, although nuclear condensation, fragmentation, and dissolution continued. TTC staining revealed both red-stained normal tissue and white-stained infarct tissue at one day post-reperfusion. At seven days post-reperfusion, the volume of white infarct tissue increased further, accompanied by swelling of brain tissue. By fourteen days post-reperfusion, the volume of white cerebral infarction tissue decreased, although brain tissue remained swollen. These findings provide crucial insights into the pathogenesis of ischemic-reperfusion injury in rats, significantly enhancing our understanding of the mechanisms underlying reperfusion injury during cerebral ischemia.These findings contribute novel insights and theoretical underpinnings for the prevention and management of reperfusion injury in cerebral ischemia.

Mengxue Zang, Xichao Zang, Jianmin Huang. A Study on the Extent of Brain Tissue Damage at Different Reperfusion Time Points Using a Rat Model of Cerebral Ischemia-Reperfusion Injury. Frontiers in Medical Science Research (2025), Vol. 7, Issue 6: 102-108. https://doi.org/10.25236/FMSR.2025.070613.

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