Abstract
The temporal evolution and spatial distribution of ischemic cell injury was investigated after transient middle cerebral artery (MCA) occlusion. Male Wistar rats ( n = 61) were subjected to 2 h of MCA occlusion induced by advancing a nylon monofilament into the right internal carotid artery. Animals were killed after different durations of reperfusion, ranging from 4 to 166 h ( n = 6–11 for each group). Neuronal injury and astrocytic reaction were evaluated using hematoxylin and eosin (H & E) and glial fibrillary acidic protein (GFAP) immunohistochemistry, respectively. Eosinophilic neurons were detected at 4 h of reperfusion in the basal ganglia, and at 10 h of reperfusion in the cortex. Focal brain infarct developed by 46 h of reperfusion, both in the cortex and the basal ganglia, and the volume remained constant between 46 and 166 h of reperfusion. Significant differences in astrocytic reaction were detected between the lesion and the periphery of the lesion at reperfusion times from 46 to 166 h; GFAP staining decreased in the core of the lesion and increased in the peripheral areas. Our data suggest that, after 2 h of MCA occlusion, brain tissue progresses from isolated neuronal injury to infarct with a time course dependent on anatomical site; and astrocytic reactivity, expressed by GFAP staining, reflects the outcome of the ischemic injury.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
