Wear of low-
oxygen-transmissible
soft contact lenses swells the cornea significantly, even during open eye. Although
oxygen-deficient
corneal edema is well-documented, a self-consistent quantitative prediction based on the underlying metabolic reactions is not available. We present a biochemical description of the human cornea that quantifies hypoxic swelling through the coupled transport of water,
salt, and respiratory metabolites. Aerobic and anaerobic consumption of
glucose, as well as
acidosis and pH buffering, are incorporated in a seven-layer corneal model (anterior chamber, endothelium, stroma, epithelium, postlens tear film,
contact lens, and prelens tear film). Corneal swelling is predicted from coupled transport of water, dissolved
salts, and especially metabolites, along with membrane-transport resistances at the endothelium and epithelium. At the endothelium, the Na+/K+ -
ATPase electrogenic channel actively transports
bicarbonate ion from the stroma into the anterior chamber. As captured by the Kedem-Katchalsky membrane-transport formalism, the active
bicarbonate-ion flux provides the driving force for corneal fluid pump-out needed to match the leak-in tendency of the stroma. Increased
lactate-ion production during
hypoxia osmotically lowers the pump-out rate requiring the stroma to swell to higher water content. Concentration profiles are predicted for
glucose, water,
oxygen,
carbon dioxide, and hydronium,
lactate,
bicarbonate, sodium, and
chloride ions, along with electrostatic potential and pressure profiles. Although the active
bicarbonate-ion pump at the endothelium drives
bicarbonate into the aqueous humor, we find a net flux of
bicarbonate ion into the cornea that safeguards against
acidosis. For the first time, we predict corneal swelling upon
soft-contact-lens wear from fundamental biophysico-chemical principles. We also successfully predict that hypertonic tear alleviates
contact-lens-induced
edema.