Experimental obstruction to aqueous outflow by pigment particles in living monkeys.

Pigment particles (1 X 10(6)/microliters) isolated from the iris and ciliary body of enucleated cynomolgus monkey eyes were infused into the anterior chamber of seven living cynomolgus monkeys and aqueous humor outflow facility determined by the two-step constant-pressure perfusion technique. Outflow facility acutely decreased 64% in the experimental pigment perfused eyes compared to a 76% increase in the sham-manipulated fellow eyes (P less than 0.001). However, when next measured 1 wk later, facility in the pigment perfused eyes had returned to baseline levels. Repetitive pigment perfusions similarly failed to produce any long-term abnormality in outflow facility. Gonioscopically, a well-defined band of pigment was observed in the trabecular meshwork, which decreased in density with time. Scanning and transmission electron microscopy documented pigment particle phagocytosis by trabecular endothelial cells and macrophages. Forty-two and 105 days after pigment infusion the trabecular meshwork was normal morphologically, and, despite an observed decrease in trabecular pigmentation, morphometry failed to reveal a decrease in trabecular meshwork cellularity in experimental compared to control eyes. These results suggest that factors other than, or in addition to, pigment particle accumulation in the trabecular meshwork must be involved in the mechanism of human pigmentary glaucoma.