LONG-TERM OBSERVATION OF MORPHOLOGIC AND FUNCTIONAL FEATURES OF CAT CORNEAL ENDOTHELIUM AFTER WOUNDING

Purpose. (1) To test the hypothesis that corneas with enlarged endothe lial cells (and thus less intercellular space) have decreased endothel ial permeability to small polar solutes. (2) To measure corneal endoth elial ouabain binding (Na+/K+ ATPase ''pump site'' density) and Descem et's membrane production after endothelial wounding. Methods. Bilatera l specular microscopy and anterior segment fluorophotometry were perfo rmed at 2-month intervals for 1 year in ten cats after mechanically da maging the corneal endothelium in one eye of each. The measurements we re repeated at 2 years in four cats and at 3 years in two cats. Eighte en months after wounding, endothelial ouabain binding was measured in both eyes of six cats. Transmission electron micrographs of Descemet's membrane were analyzed in both eyes of six cats at 18 months, two cat s at 2 years, and two cats at 3 years after wounding. Results. From 6 to 12 months after wounding, the endothelial permeability to carboxyfl uorescein was significantly decreased (P < 0.05), and the mean endothe lial cell size was significantly increased (P < 0.001) in the damaged eyes. The enlarged endothelial cells persisted in the few cats observe d 2 and 3 years after wounding. There was no significant difference in endothelial ouabain binding between the damaged and control corneas i n six cats tested 18 months after wounding. On subsequent histologic e xamination, a layer of abnormal Descemet's membrane was present in all ten wounded eyes, with additional normal Descemet's membrane posterio r to it, between the abnormal layer and the endothelial cells. Conclus ions. The results are consistent with the hypothesis that corneal endo thelial permeability to small polar solutes varies directly with the a mount of intercellular space available for diffusion across the monola yer. The results also confirm clinical reports of decreased endothelia l permeability in corneas with enlarged endothelial cells. In histopat hologic specimens, a layer of abnormal Descemet's membrane can be a hi storical marker for a period of endothelial damage and corneal decompe nsation.