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Brian K. Leung, Joseph A. Bonanno, Clayton J. Radke; Oxygen-Deficient Metabolism And Corneal Edema. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1092.
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Wear of low oxygen-transmissible (Dk/L) contact lenses swells the cornea significantly, even during open eye. This research quantitatively assesses hypoxic corneal edema using fundamental concepts from cell biology and metabolism.
A steady-state, seven-layer mathematical model was used to study solute transport and swelling associated with the wear of contact lenses of varying Dk/L. We account for aerobic and anaerobic respiration as well as bicarbonate buffering. The metabolites are carbon dioxide, oxygen, glucose, and lactate, hydrogen, bicarbonate ions. We also include sodium ions, chloride ions, and water. The pump-leak mechanism of Maurice is accounted for through endothelial and epithelial membrane transport using known cell biology. Mass transport in the other layers is treated by dilute-solution theory. Monod reaction rates, membrane coefficients, and anterior chamber and tear-film compositions are from the literature.
Model predictions of corneal swelling during open- and closed-eye SCL wear for Dk/L values ranging from 0 to 140 hBarrer/cm are in agreement with the experiments of Holden and Mertz. Of the 5% corneal swelling predicted for the no-lens closed eye, we attribute about 40% to hypoxia and the remaining 60% to open-eye tear-film osmolarity. Based on known active endothelial bicarbonate pump rates, we predict a net bicarbonate influx across the endothelium and into the cornea to maintain physiological pH of near 7.6. Inhibition of the bicarbonate buffering in the cornea results in over-acidosis with pH values near 3.
For the first time, we predict Holden-Mertz curves quantitatively from first principles. Tear-film osmotic effects and hypoxia each contribute to corneal swelling. Contrary to previous work, we predict a net bicarbonate influx across the endothelium to mitigate hydrogen ions produced from anaerobic respiration.
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