Initial Clinical Experience with the Intracavernous Application of the Nitric Oxide Donor Sin 1 in the Treatment of Patients with Erectile Dysfunction

Abstract

Penile erection requires a series of events that includes cavernous and vascular smooth muscle relaxation, increased arterial inflow and subsequent venous outflow restriction. Recent work suggests that the initial step, cavernous and vascular smooth muscle relaxation, is mediated by the synthesis and release of nitric oxide from nerves innervating vascular and cavernous smooth muscles (Ignarro et al., 1990; Holmquist et al., 1991; Rajfer et al., 1992; Burnett et al., 1992). Therefore, the use of the L-arginine/nitric oxide pathway seems to be a possible approach in the treatment of erectile dysfunction. Linsidomine chlorhydrate (SIN-1, Corvasal intracoronaire^®), the active hepatic metabolite of molsidomine (N-ethoxycarbomyl-3-morpholino- sydninimine), is believed to liberate nitric oxide nonenzymatically (nitric oxide donor). Theoretically, a nitric oxide donor may be superior to other vasoactive drugs because it may resemble more closely the physiologic sequence of events in penile erection. Our preliminary results with the intracavernous application of SIN-1 suggested a possible role in the treatment of patients with erectile dysfunction (Stief et al., 1992). We now report our extended follow up with SIN-1 in the diagnosis and treatment of patients with erectile dysfunction.