Effect of iodoacetamide perfusion on outflow facility and metabolism of the trabecular meshwork.

Freshly enucleated eyes were quantitatively perfused via the anterior chamber with varying dosages of iodoacetamide at constant pressure. Iodoacetamide caused a significant increase in facility of outflow in a dose-response manner in calf and monkey eyes. Almost complete inhibition of glycolysis in the calf trabecular meshwork was produced by a dosage of iodoacetamide that was too low to appreciably alter the facility. A similar response was produced by a higher dosage, which did significantly increase the facility. Our results, taken together with what is known of the properties of iodoacetamide, suggest that cellular sulfhydryl groups may be involved in a mechanism for aqueous flow through the trabecular meshwork and that iodoacetamide probably acts directly on cellular permeability rather than by inhibition of glycolysis or interference with the production of energy in the trabecular meshwork.