EFFECT OF NITRIC OXIDE-DONOR, LINSIDOMINE CHLORHYDRATE, IN TREATMENT OF HUMAN ERECTILE DYSFUNCTION CAUSED BY VENOUS LEAKAGE

Recent experimental work has demonstrated that nitric oxide (NO) is th e neurotransmitter responsible for cavernous smooth muscle relaxation. We studied the effect of a direct NO-donor, linsidomine chlorhydrate (SIN-1), in 30 patients with venous leakage confirmed by dynamic pharm acocavernosography and pharmacocavernosometry that was refractory to p rostaglandin E1 (PGE1) under the assumption that the more physiologic approach might give better results. In all 30 patients, response to SI N-1 was no better, and in 22 cases it was less than the response to PG E1. No systemic or local side effects of SIN-1 were observed. SIN-1 is not superior to PGE1 in the treatment of erectile dysfunction caused by venous leakage, and failure of NO-mediated smooth muscle relaxation does not play a part in the entity, ''venous leakage.''