ENDOTHELIAL BARRIER FUNCTION AND NA+ K+-ATPASE PUMP DENSITY IN HERPETIC STROMAL DISEASE/

Purpose. Corneal edema is a significant component of the various forms of herpes simplex virus type 1 (HSV-1)-induced stromal disease. Maint enance of corneal thickness, a reflection of corneal hydration, depend s on a physical barrier formed by endothelial cell-cell junctions and by the activity of Na+/K+-ATPase pumps that regulate ion flux and thus influence water movement through this cell layer. These functions wer e measured in corneas with increased corneal thickness caused by HSV-1 -induced stromal disease to determine their contribution to the pathog enesis of the edema. Methods. Stromal disease with corneal edema was i nduced in rabbits by intrastromal injection of the RE strain of HSV-1. At various times after infection, during the development of and recov ery from stromal disease, endothelial barrier function and Na+/K+-ATPa se pump sites were measured in excised rabbit corneas. Results. The en dothelial permeability coefficient, K-trans, for C-14-dextran, H-3-inu lin, and C-14-mannitol, were not altered significantly during periods of maximal corneal edema and stromal disease. Endothelial Na+/K+-ATPas e pump density, as measured by ouabain binding, showed a statistically significant (P < 0.05) decrease in HSV-1-infected corneas during peak edema compared to mock antigen-injected or uninjected control corneas . Pump density returned to baseline values by 24 days after infection, concurrent with the resolution of corneal edema. Conclusions. These r esults indicate that corneal endothelial barrier function was not alte red in this form of HSV-1-induced stromal edema; however, pump density was reduced significantly.