Materials and Methods: Sixteen male Wistar-Albino rats weighing 200-250 mg were kept in a stable environment at a constant room temperature and humidity and were divided into study (n=8) and control (n=8) groups. IR injury is induced in right eye of the study group via increasing intraocular pressure to 110 mmHg for 60 minutes. Both eyes of the study and the control group were enucleated and analyzed with hematoxylene-eosin (H&E) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) stainings. Retinal thickness measurements performed in H&E sections were compared between and within groups. TUNEL staining was used to evaluate apoptosis.

Results: There was no significant difference between right and left eye of the control group (143.9±4.2 μm and 143.3±3.5 μm respectively, p=0.74). IR had resulted in increment of retinal thickness in the IR eye (228.7±13.1 μm) and fellow non-ischemic eye (166.72±9.7 μm) of the study group and the change was statistically significant when compared to the control group (p<0.01). Compared to the control group, TUNEL staining revealed increased number of apoptotic cells in the IR eye but not in the fellow non-ischemic eye.

Conclusion: IR resulted in involvement of fellow eye demonstrated with increased retinal thickness but not caused enough changes to develop apoptosis. Setting the fellow eye in retinal IR injury model is not appropriate. Keywords : Ischemia reperfusion, animal, retinal thickness, apoptosis