J J Bookstein

Penile Pharmacocavernosography and Cavernosometry in the Evaluation of Impotence

Within the past few years, veno-occlusion of the corpora cavernosa has become generally recognized as an essential prerequisite for adequate penile erection. Veno-occlusive incompetence is suspected to be a frequent cause of impotence. Our recent experience with cavernosography in two normal volunteers and 36 impotent patients indicates that angiography is reliable in evaluating the competence of the veno-occlusive mechanism only if both pharmacocavernosography (PCG) and pharmacocavernosometry (PCM) are applied. Twenty minutes after intracavernosal (IC) injection of a mixture of 60 mg. papaverine and one mg. phentolamine (regitine), 100 ml. of diluted radiographic contrast medium are infused at the rate of one or two ml./sec. while pressure is recorded, and radiographic films are exposed at the rate of one every eight to 15 seconds. PCM and PCG of the corpora cavernosa indicated the overall degree of competence of the cavernosal veno-occlusive mechanisms, and the sites of veno-occlusive incompetence; non-pharmacologic studies were unreliable in these regards. During non-pharmacologic infusion in normals, pressures rose to 40 to 45 mm. Hg, and free efflux could be visualized from multiple venous systems. After pharmacologic injection in normals, all venous channels closed, and pressures rapidly rose toward or above 200 mm. Hg, at which time the infusion was stopped. Veno-occlusive incompetence was defined angiographically when more than minimal efflux occurred during pharmacocavernosography from any venous system. The incompetence could involve the deep penile system, the deep dorsal system, or the spongiosal system, alone or in combination. Severe veno-occlusive incompetence was considered diagnostic of venogenic impotence, and was defined manometrically when IC pressures failed to exceed 100 mm. Hg during infusion of 100 ml. of fluid at 2 mm./second after IC papaverine and phentolamine injection. We believe these angiographic methods will improve the criteria against which other diagnostic and therapeutic methods can be assessed.

Production of Penile Veno-Occlusive Insufficiency by Arterial Occlusion in a Canine Model

Angiographic evaluation of impotent men revealed a frequent association between penile arterial disease and veno-occlusive insufficiency of the corpora cavernosa. In order to evaluate a possible cause-and-effect relationship, we investigated the competence of the cavernosal veno-occlusive mechanism in a canine model at various intervals after onset of cavernosal ischemia. In most dogs, the veno-occlusive mechanism could no longer be activated by papaverine after about 30 minutes of ischemia. If ischemia was relieved shortly thereafter, veno-occlusive competence returned after a further delay of one or two hours. The evidence suggests that veno-occlusive failure is not simply a hemodynamic consequence of loss of arterial inflow, but instead secondary to some ischemic injury. We conclude that arterial insufficiency may be one of the causes of cavernosal veno-occlusive insufficiency in humans.

The Veno-Occlusive Mechanism of the Canine Corpus Cavernosum: Angiographic and Pharmacologic Studies

Studies were designed to document the normal angiography and pressure-volume characteristics of the canine corpus cavernosum, evaluate the effects of various vasoactive agents, and characterize a veno-occlusive mechanism. In fourteen dogs, baseline cavernosography demonstrated venous drainage via six to ten tributaries arising from the crura and entering the deep penile veins. Control cavernosometry during infusion of saline at 0.33 ml./sec. led to a rise in intracavernosal pressure (ICP) from 24.9 +/- 7.9 mm. Hg to 68.4 +/- 21.1 mm. Hg. Intracavernosal injection of a number of vasodilators, including papaverine, nitroglycerin, acetylcholine, and prostaglandin E2, raised baseline ICP significantly, caused extreme elevation of pressure during saline infusion (greater than 450 mm. Hg), and narrowed or obliterated the venous lumena at the site of tunica perforation, as judged angiographically. These effects could be reversed with phenoxybenzamine or norepinephrine. Our results further support the current understanding of the canine veno-occlusive mechanism.