In vivo Assessment of Mechanisms Controlling Corneal Hydration

摘要

Both passive and active mechanisms function in control of corneal hydration. These mechanisms have primarily been determined from in vitro animal studies; however, the mechanisms controlling human corneal hydration have yet to be assessed. To investigate these mechanisms, corneal hydration was increased using a contact lens induced hypoxic stress. Following lens removal, the rate of corneal thickness recovery was monitored under various environmental conditions. Recovery of the cornea to baseline thickness follows a nonlinear time course, with the rate of recovery decreasing as the cornea thins. For initial swelling of 40-54 micrometers, 55-69 micrometers and 70 micrometers and above, the time to reach baseline thickness was 1.5, 2.0, and 2.5 hours, respectively. The active endothelial pump and passive evaporation components of this recovery were studied by inducting edema and monitoring the subsequent decrease in corneal thickness both with and without evaporation during open and closed eye conditions, respectively. Endothelial function may be affected by the endothlial cell loss and increased variability in cell shape and size (polymegathisms) that accompany aging. Age-related changes in endothelial function were assessed by comparing the corneal recovery and endothlial morphology between a group of younger (mean age, 26.7 yrs) and older (65.7 yrs) subjects who are free of clinically assessible corneal disease.