N-ethylmaleimide increases the facility of aqueous outflow of excised monkey and calf eyes.

Freshly enucleated eyes were quantitatively perfused via the anterior chamber at 15 mm Hg pressure with various concentrations of the sulfhydryl (-SH) agent. N-ethylmaleimide (NEM). In the monkey eye a dosage of 9.4 mM NEM produced a 108% increase in facility of outflow. In calf eyes a dosage of NEM of 4.7 mM or greater also produced a significant increase in outflow facility. At the threshold dosage of 4.7 mM NEM there was only slight (12%) inhibition of glycolysis in the calf meshwork, which was excised after perfusion. The results suggest that the effect of NEM on outflow facility is not caused by a metabolic inhibitory action. We propose that alteration of cell membrane -SH groups in the outflow pathways can influence aqueous outflow resistance.