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269 HYPEROXIA ALTERS ENDOTHELIAL CELL PROLIFERATION

Retinopathy of prematurity (ROP) is characterized by an early vaso-obliterative stage which can be seen experimentally during periods of hyperoxia and a later stage of neovascularization which follows the period of high oxygen exposure. Because endothelial cell proliferation is an important step in neovascularization, we have examined the effects of varying oxygen tensions on endothelial cell proliferation in vitro. Fetal bovine aortic endothelial cells (FBAE) were plated at a density of 40,000 cells/35mm culture dish and maintained in 20% O2/75% N2/5% CO2 at 37°C. After 48 hours, FBAE were exposed to 95% O2/5% CO2 (hyperoxia) or 20% O2/75% N2/5% CO2 (control) at 37°C for 48 hours. Following oxygen exposure, all cells were placed in 20% O2/75% N2/5% CO2 at 37°C and followed for 7 days. pH and PCO2 of the media were maintained at 7.4 and 30-37 torr respectively. Cell counts were performed daily (Coulter Counter). In cells exposed to 48 hours of hyperoxia, FBAE growth ceased (100% inhibition) while control cells continued to proliferate. When oxygen-exposed FBAE were returned to a normoxic environment, they again proliferated, with growth rates now approximating that of control cells. During limited periods of hyperoxia, FBAE growth is arrested. In a normoxic environment, O2-exposed FBAE again proliferate. Direct effects of hyperoxia on vascular endothelial cell proliferation may play a role in the vascular changes of ROP.