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 the 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 pharmacocavernosography and pharmacocavernosometry that was refractory to prostaglandin E1 (PGE1) under the assumption that the more physiologic approach might give better results. In all 30 patients, response to SIN-1 was no better, and in 22 cases it was less than the response to PGE1. 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."
Wegner
H E
HE
Department of Urology, Universitätsklinikum Steglitz, Freie Universität Berlin, Germany.
Knispel
H H
HH
D000328:Adult; D000368:Aged; D000527:Alprostadil / Q000627:therapeutic use; D007172:Erectile Dysfunction / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000627:therapeutic use; D009569:Nitric Oxide / Q000378:metabolism; D014652:Vascular Diseases / Q000150:complications; D014665:Vasodilator Agents / Q000627:therapeutic use*; D014680:Veins
D014665:Vasodilator Agents; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine; D000527:Alprostadil