Abstract
PURPOSE. To measure the specific hydraulic conductivity (K) of human sclera over a range of ages, to assess topographical variation, and to provide a theoretical estimate of potential scleral outflow facility. METHODS. Human donor sclera (n = 18; mean age 56.7 +/- 25.9 years; range 4-89) was clamped in a modified Ussing chamber connected to a water column set at 15.7 mm Hg. Column descent was ...
Abstract
PURPOSE. To measure the specific hydraulic conductivity (K) of human sclera over a range of ages, to assess topographical variation, and to provide a theoretical estimate of potential scleral outflow facility. METHODS. Human donor sclera (n = 18; mean age 56.7 +/- 25.9 years; range 4-89) was clamped in a modified Ussing chamber connected to a water column set at 15.7 mm Hg. Column descent was measured over 24 hours at 20 degrees C with a digital micrometer. Scleral thickness of glutaraldehyde-fixed specimens was measured by light microscopy, taking the mean of 15 measurements per donor. Topographical variation in hydraulic conductivity (HC) was determined in an additional 10 donor eyes (mean age, 54.1 +/- 26.4 years; range 12-89), comparing anterior, equatorial, and posterior sclera. The potential transscleral outflow facility was calculated by multiplying HC by total scleral surface area and adjusting water viscosity to core body temperature. RESULTS. Mean K +/- 1SD in adults (> 18 years) was 5.85 +/- 3.89 x 10(-18) m(2). K tended to be higher in pediatric donors, but there was no statistically significant age-related change. However, when all data sets were combined (n = 28), HC showed a significant decline with age. There was no significant topographical variation in HC. The potential transscleral outflow facility was 0.33 mu L (.) min(-1) (.) mm Hg-1. CONCLUSIONS. Quantifying HC may help refine ocular pharmacotherapy, as transscleral water movement increases intraocular drug elimination and impedes transscleral drug delivery. The potential scleral outflow is two to three times higher than that which occurs in vivo; hence, medical or surgical interventions that fully exploit this pathway have considerable capacity to lower intraocular pressure.
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