Abstract

The rate of oxygen consumption is an important parameter to assess the physiology of the human cornea. Metabolism of oxygen in the cornea is influenced by contact-lens-induced hypoxia, diseases such as diabetes, surgery, and drug treatment. Therefore, estimation of in vivo corneal oxygen-consumption rate is essential for gauging adequate oxygen supply to the cornea. Phosphorescence quenching of a dye coated on the posterior of a soft contact lens provides a powerful technique to measure tear-film oxygen tension (Harvitt and Bonanno, Invest Ophthalmol Vis Sci 1996;37:1026-1036; Bonanno et al., Invest Ophthalmol Vis Sci 2002;43:371-376). Unfortunately, previous work in establishing oxygen-consumption kinetics from transient postlens tear-film oxygen tensions relies on the simplistic assumption of a constant corneal-consumption rate. A more realistic model of corneal metabolism is needed to obtain reliable oxygen-consumption kinetics. Here, physiologically relevant nonlinear Monod kinetics is adopted for describing the local oxygen-consumption rate, thus avoiding aphysical negative oxygen tensions in the cornea. We incorporate Monod kinetics in an unsteady-state reactive-diffusion model for the cornea contact-lens system to determine tear-film oxygen tension as a function of time when changing from closed-eye to open-eye condition. The model was fit to available experimental data of in vivo human postlens tear-film oxygen tension to determine the corneal oxygen-consumption rate. Reliance on corneal oxygen diffusivity and solubility data obtained from rabbits is no longer requisite. Excellent agreement is obtained between the proposed model and experiment. We calculate the spatial-averaged in vivo human maximum corneal oxygen-consumption rate as Q(c)(max) = 1.05 x 10(-4) mL/(cm(3) s). The calculated Monod constant is K(m) = 2.2 mmHg.

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