Purpose: The authors investigated whether regulation of the trabecular extracellular matrix turnover rate and remodeling plays an important role in decreasing outflow resistance by determining the effect of intracamerally given interleukin-1alpha, a known stimulator of the expression of trabecular matrix metalloproteinases, on outflow facility of albino rat eyes.
Materials and methods: Forty normal albino rats (Sprague-Dawley), weighing 250 to 300 g, were studied. Rats were anesthetized by intraperitoneal pentobarbital sodium (30 mg/kg) injection. The rats were separated into four groups and given 5, 10, 25, or 50 units of interleukin-1alpha injected intracamerally in one eye. Bovine serum albumin in phosphate-buffered saline, which was used to dissolve the interleukin-1alpha, was injected in the fellow eye as a control. Outflow facility was measured by two-level constant pressure perfusion 1, 3, and 7 days after injection.
Results: The eyes treated with 50 units of interleukin-1alpha showed a statistically significant increase of outflow facility by 37% compared with the contralateral control eyes 3 days after injection, but returned to normal levels in 7 days. The eyes treated with 5, 10, 25, or 50 units of interleukin-1alpha showed outflow facility increases of 12%, 20%, 39%, and 37%, respectively, 3 days after injection.
Conclusion: Interleukin-1alpha increased the outflow facility, supporting the hypothesis that regulation of trabecular meshwork extracellular matrix plays a role in trabecular outflow resistance.