Long-term observation of morphologic and functional features of cat corneal endothelium after wounding.
OBJECTIVE
(1) To test the hypothesis that corneas with enlarged endothelial cells (and thus less intercellular space) have decreased endothelial permeability to small polar solutes. (2) To measure corneal endothelial ouabain binding (Na+/K+ ATPase "pump site" density) and Descemet's membrane production after endothelial wounding.


METHODS
Bilateral specular microscopy and anterior segment fluorophotometry were performed at 2-month intervals for 1 year in ten cats after mechanically damaging the corneal endothelium in one eye of each. The measurements were repeated at 2 years in four cats and at 3 years in two cats. Eighteen 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 cats at 2 years, and two cats at 3 years after wounding.


RESULTS
From 6 to 12 months after wounding, the endothelial permeability to carboxyfluorescein was significantly decreased (P < 0.05), and the mean endothelial cell size was significantly increased (P < 0.001) in the damaged eyes. The enlarged endothelial cells persisted in the few cats observed 2 and 3 years after wounding. There was no significant difference in endothelial ouabain binding between the damaged and control corneas in six cats tested 18 months after wounding. On subsequent histologic examination, a layer of abnormal Descemet's membrane was present in all ten wounded eyes, with additional normal Descemet's membrane posterior to it, between the abnormal layer and the endothelial cells.


CONCLUSIONS
The results are consistent with the hypothesis that corneal endothelial permeability to small polar solutes varies directly with the amount of intercellular space available for diffusion across the monolayer. The results also confirm clinical reports of decreased endothelial permeability in corneas with enlarged endothelial cells. In histopathologic specimens, a layer of abnormal Descemet's membrane can be a historical marker for a period of endothelial damage and corneal decompensation.
Bourne
W M
WM
Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota 55905.
Nelson
L R
LR
Buller
C R
CR
Huang
P T
PT
Geroski
D H
DH
Edelhauser
H F
HF
D000818:Animals; D002415:Cats; D002452:Cell Count; D002463:Cell Membrane Permeability; D003886:Descemet Membrane / Q000648:ultrastructure; D004728:Endothelium, Corneal / Q000293:injuries / Q000473:pathology* / Q000503:physiopathology; D005131:Eye Injuries / Q000473:pathology* / Q000503:physiopathology; D005452:Fluoresceins / Q000378:metabolism; D015590:Fluorophotometry; D008137:Longitudinal Studies; D010042:Ouabain / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014945:Wound Healing / Q000502:physiology*
D005452:Fluoresceins; C024098:6-carboxyfluorescein; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase