EXPERIMENTAL RETINOPATHY BY HYPERBARIC OXYGENATION

Retinopathy of prematurity (ROP) usually occurs after a prolonged expo sure to normobaric hyperoxia in newborn mammals and infants. We hypoth esized that experimental ROP also could develop after acute exposures to hyperbaric oxygenation (HBO), providing that a severe and maintaine d retinal vasoconstriction occurred during HBO exposure. Five- to seve n-day-old, Long Evans Sprague-Dawley rats were exposed for 5 h either to 5 atm abs oxygen or to 5 atm abs O-2 with 190 mmHg inspired PCo2, ( hypercapnia). Control rats breathed air at atmospheric pressure. Two m onths after exposures, rats were anesthetized, perfused intraventricul arly with India ink, and retinal images were obtained. Retinal vascula r density (RVD) in each image was calculated as the number of pixels i n the retinal vessel area divided by the total number of pixels in the image (retinal tissue and vessels). The RVD was significantly increas ed from 0.0112 +/- 0.004 in the air-exposed controls to 0.0417 +/- 0.0 29 in the HBO-exposed rats (mean +/- SD; n = 4 in each group). HBO wit h hypercapnia produced a nonsignificant increase in RVD (0.0255 +/- 0. 007; n = 4), reducing the HBO-induced increase in RVD by 39%. These re sults are consistent with the hypothesis that a sustained HBO-induced retinal vasoconstriction in newborn rats, followed by a hypoxic-ischem ic injury, might result in vascular proliferation, thereby initiating ROP development on return to air. Hypercapnia does not completely prev ent HBO-induced retinal vasoproliferation, probably because possible v asodilation, induced by hypercapnia, can greatly elevate retinal tissu e Po,and promote oxidative damage.