Abstract

Currently prevailing opinion on the mechanism of corneal deturgescence (stromal thinning) is that it is a process mediated by an endothelium-sited fluid pump. This pump is considered to be bicarbonate-dependent and balanced by the passive tendency of the stroma to absorb fluid that leaks from the aqueous across the endothelium. A case is presented that the utility of older key experiments as supportive evidence for this bicarbonate pump is limited by methodological errors in the formulation and use of bicarbonate-containing solutions. Recent studies reveal the pump to be generally unaffected by exogenous bicarbonate levels. Several recent studies confirm that the deturgescence of stroma-endothelium preparations is remarkably sensitive to exogenous bicarbonate and further indicate that the actual hydration of the stroma is inversely related to exogenous bicarbonate levels. These studies also show that it is possible to observe deturgescence in stroma-endothelial preparations which have no apparent net fluid pump activity. Conversely, net fluid pump activity has been measured in preparations which nonetheless fail to show deturgescence. Therefore, there does not appear to be an obligate coupling between deturgescence and endothelial fluid pump activity. The possible role of the endothelium in regulating the bicarbonate movement into the collagen-keratocyte matrix of the corneal stroma (rather than pumping it out) is discussed as a possible interpretation of more recent data.

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