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Abstract
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.