Abstract
The effect of increased intraocular pressure (IOP) on stimulated aqueous humor flow (AHF) was studied in cynomolgus monkeys. Two experimental series were performed, one with unilateral VIP-treatment (60 micrograms intracamerally) and one with unilateral terbutaline-treatment (10 micrograms.ml-1 perfusion fluid). The AHF was determined with a labelled albumin dilution method, and an artificial increase in IOP was produced by clamping the outlet of the perfusion system, thus causing a net inflow of perfusion fluid. The initial AHF was significantly higher in the VIP-treated eye than in the control eye - 1.568 +/- 0.095 as compared to 1.112 +/- 0.103 microliters.min-1 (P less than or equal to 0.01). The spontaneous IOP was 5.8 +/- 0.4 mmHg (P less than or equal to 0.001) higher in the VIP-treated eye. There was no difference in pseudofacility between the VIP-treated eye (0.063 +/- 0.016 microliter.min-1.mmHg-1) and the control eye (0.065 +/- 0.022 microliter.min-1.mmHg-1), but the total and true outflow facilities were higher in the VIP-treated eye. In the experiments with terbutaline, the initial AHF was 1.729 +/- 0.114 for the experimental eye and 1.262 +/- 0.104 microliters.min-1 for the control eye (P less than or equal to 0.01). The pseudofacility tended to be higher in the terbutaline-treated eye (0.072 +/- 0.026 microliters.min-1.mmHg-1) than in the control eye (0.048 +/- 0.012 microliters.min-1.mmHg-1), but the difference was not statistically significant. There was no difference in total and true outflow facility between the experimental and control eye. The results indicate that the pressure sensitivity of the AHF is independent of the initial level of the AHF. VIP increases true outflow facility, possibly via a direct effect on the trabecular meshwork. VIP also appears to rise the IOP due to an increase in episcleral venous pressure, which could be secondary to vasodilatation in the anterior segment.
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