Recent studies on the nature and function of the corneal endothelial barrier

The development of new perfusion procedures, the development of new colloidal tracer techniques and the application of the concept of pump-leak to the corneal endothelium has led us to reinvestigate several aspects of the barrier function of the corneal endothelium. A barrier to free diffusion of fluids across the endothelium can be demonstrated in corneas perfused in vitro under a variety of conditions. This barrier can be reduced or abolished by perfusion with a Ca 2+-free medium, eye-bank type storage, and perfusion at increased perfusion (intraocular) pressures. In the first instance a clear morphological basis for the loss of barrier function, the disintegration of the endothelial junctional complex, is easily demonstrable. Both the physiological and morphological effects of Ca 2+-free perfusion are reversible within limits. In the other two instances of reduced barrier function no clear morphological correlate has yet been demonstrated. In fact, the apical membrane, apical junction and apical microfilament network appear to be particularly resistant to the damage caused by storage of corneas at 4°C. The application of new colloidal tracer techniques involving horseradish peroxidase and lanthanum nitrate to the study of the endothelial junction have shown that this is not a tight junction and that particles as larga as 3 nm can penetrate the apical junctional zone in rabbit and monkey. The present report reviews and summarizes the work of our laboratory during the past several years and indicates some of the still unanswered questions concerning the endothelial barrier. In addition, we suggest some pathways of investigation which we believe would be particularly fruitful at this time.