This content is PDF only. Please click on the PDF icon to access.
Abstract
Enucleated calf and primate eyes were perfused with either p-chloromercuribenzene sulfonate (PCMBS) or p-chloromercuribenzene (PCMB). Both caused a decrease in aqueous outflow that did not result from inhibition of glycolysis in trabecular cells. Morphologic studies of PCMBS-treated primate eyes suggested that the reduction in aqueous outflow occurred as the result of cellular swelling in the trabecular meshwork and, particularly, in the juxtacanalicular connective tissue. These findings suggest that changes in cell volume may influence trabecular outflow resistance and that mercurial-sensitive membrane sulfhydryl groups could participate in the regulation of aqueous outflow.