Corneal endothelial structure and function under normal and toxic conditions.
Our understanding of the function of the corneal endothelium in corneal thickness regulation, and the role of ion transport mechanisms in endothelial physiology, has expanded greatly over the past 25 years. The basic events occurring across the apical and basolateral membranes of the cells are far better understood today, although gaps still exist in the area of the relationship of the cellular and paracellular pathways and their relative contribution to the overall behavior of the endothelium. Little is known about the movement of ions or fluid between the cells or in what proportion this may occur compared to the cellular events. Furthermore, although our knowledge of the ionic movement processes has been enhanced, the link between fluid transfer across the endothelium and ion movements remains an enigma. Important questions also remain concerning the link between electrical characteristics and either ion movement or fluid transport. Improved storage solutions are needed that will preserve endothelial function after transplantation through the provision of a significant improvement in long-term cell survival. The limit to preservation time at present is about 14 days, and the use of other variables in the storage solution may extend this time. In reality, however, extension of preservation time is now of secondary importance relative to the need to enhance cell survival and reduce cell loss following surgery. Whether such improvement can be made with manipulation of the solution alone, or whether refinements are needed in the surgical technique awaits further study. Our comprehension of the biochemical linkage between energy supply and ion movement also remains uncertain in view of the particular intracellular localization of the anionic ATPases to mitochondrial loci. Despite numerous attempts there have been only a few chemicals identified that stimulate the fluid pump, but the level of stimulation has been relatively small and short-lived. No sustained effects have been found that would be of clinical benefit in reducing corneal thickness. A considerable variety of chemicals has been tested on the endothelium and it is unlikely that any new compounds will be identified that will cause enhancement of the fluid pump that would be of clinical benefit in dystrophic, or otherwise swollen, corneas. Of all the toxic responses of the endothelium the majority have been identified because of a malfunction of corneal thickness regulation, with the resultant corneal swelling, or by morphological examination. Only in a few instances has the permeability to non-electrolytes (carboxyfluorescein, inulin/dextran) been measured, and even more rarely have ion fluxes, or pump activity (3H-ouabain binding), been measured.(ABSTRACT TRUNCATED AT 400 WORDS)
Green
K
K
Department of Ophthalmology, Medical College of Georgia, Augusta 30912-3400.
D000818:Animals; D001692:Biological Transport; D003261:Contact Lenses / Q000009:adverse effects; D015715:Corneal Edema / Q000209:etiology / Q000503:physiopathology; D004563:Electrochemistry; D004728:Endothelium, Corneal / Q000166:cytology / Q000502:physiology*; D006801:Humans; D009883:Ophthalmic Solutions / Q000633:toxicity
D009883:Ophthalmic Solutions