Experimental perforating injury with high energy electrons to inhibit intraocular proliferation.

Since 1980, the fibroblast model creating experimental proliferative vitreoretinopathy has been used to evaluate the antiproliferative effect of various drugs. In previous studies radiation therapy was found to reduce effectively intraocular proliferation in this model. We therefore investigated the effect of high energy electrons in a standard perforating injury model creating a traumatic proliferative vitreoretinopathy. In 36 eyes we performed a 8 mm pars plana incision and injected 0.4 ml of 80% fibronectin solution intravitreally. Ten rabbits (20 eyes) received radiation therapy with a Betatron accelerator in a total dosage of 3000 cGy to each eye divided into 10 single fractions starting on the first post-operative day. Maximum concentration of the dose was focused to the posterior vitreous. The other 9 rabbits, 18 eyes, served as control. In our perforating injury model we observed a reduction of retinal detachment rate of 72% in the controls to 55% in the treated group. The effect of radiation therapy with high energy electrons and total dosage of 3000 cGy was not statistically significant in experimental traumatic proliferative vitreoretinopathy.