A photothrombotic ring stroke model in rats with remarkable morphological tissue recovery in the region at risk

The photothrombotic ring stroke model with sustained underperfusion followe d by late spontaneous reperfusion (Gu et al. 1999) was employed to study it s morphological consequences. The exposed crania of adult male Wistar rats were subjected to a ring-shaped laser irradiation beam simultaneously with intravenous erythrosin B infusion. The ischemic volume was calculated from serial sections throughout the ischemic lesions at 4, 10, 24, 48, and 72 h and 7 days and 28 days after irradiation. The ischemic volume, expressed as a percentage of the ipsilateral hemispheric volume, increased steadily fro m 4 to 10 to 24 h to reach its maximum value at 48 h after irradiation; at 3 days, 7 days, and 28 days, the ischemic volume was reduced to 75%, 24%, a nd 22% of the value at 48 h. Evaluation of ischemic volumes at different an teroposterior levels revealed that the reduced ischemic volume at 72 h and later was mainly due to morphological restoration in the centrally located, nonirradiated region at risk. An initial enlargement and development of cy stic coagulation necrosis was observed in the cortical areas corresponding to the ring lesion itself. In the region at risk, a gradually deteriorating neuropil and nerve cell morphology were observed over time, with maximum s everity at 48 h postirradiation. At this time, most laminae II and III neur ons in the region at risk exhibited eosinophilia and pyknosis but no incrus tations, with small islands of less damaged neurons randomly scattered. At 72 h and up to 28 days after irradiation, these cell characteristics were n o longer observed and the region at risk was well populated with neurons th at had a chiefly unremarkable cytological appearance. Neuronal counts in th e central part of the region at risk were performed; no significant differe nce in neuronal density was observed between sham-operated controls and at 28 days after irradiation. In conclusion, the consistent, late spontaneous reperfusion coincided with remarkable tissue recovery as assessed morpholog ically in the region at risk. The data suggest that nerve cell repair may o ccur even after the detection, by conventional morphological methods, of pr olonged critical ischemic neuronal damage in the setting of acute ischemic stroke.