Oxygen is essential for aerobic mammalian cell physiology. Oxygen tension (PO2) should reach a minimum at some position within the corneal stroma, and oxygen flux should be zero, by definition, at this point as well. We found the locations and magnitudes of this “corneal equilibrium flux” (xmin) and explored its physiological implications.
We used an application of the Monod kinetic model to calculate xmin for normal human cornea as anterior surface PO2 changes from 155 to 20 mmHg.
We find that xmin deepens, broadens, and advances from 1.25 [mu]m above the endothelial-aqueous humor surface toward the epithelium (reaching a position 320 [mu]m above the endothelial-aqueous humor surface) as anterior corneal surface PO2 decreases from 155 to 20 mmHg.
Our model supports an anterior corneal oxygen flux of 9 [mu]L O2 [middle dot] cm-2 [middle dot] h-1 and an epithelial oxygen consumption of approximately 4 [mu]L O2 [middle dot] cm-2 [middle dot] h-1. Only at the highest anterior corneal PO2 does our model predict that oxygen diffuses all the way through the cornea to perhaps reach the anterior chamber. Of most interest, corneal oxygen consumption should be supported down to a corneal surface PO2 of 60 to 80 mmHg but declines below this range. We conclude that the critical oxygen tension for hypoxia induced corneal swelling is more likely this range rather than a fixed value.