Hemodynamic mechanisms of erection in the canine penis

Abstract

The hemodynamic alterations underlying erection of the canine penis were investigated utilizing electrical stimulation of the pelvic nerve. Dorsal arteries of the penis were perfused at constant flow and venous flow was measured from the dorsal veins. It was demonstrated that although dorsal vein pressure rises, obstruction of venous drainage produced either by mechanical means or by active venous constriction probably plays little or no role in the erectile process. The erection appears to be produced by a large decrease in penile arterial resistance which leads to an increase in blood flow. The magnitude of increased flow appeared to be sufficient to fill the erectile tissue and maintain filling by establishment of a new steady state of elevated blood flow. The increased flow through the penis is carried primarily through the deep arteries. Atropine reduced, but did not abolish the response to pelvic nerve stimulation. Acetylcholine administration failed to produce any signs of erection. It was postulated that acetylcholine may not be directly responsible for the vasodilatation associated with erection, but rather may serve as an intermediate in the liberation of an unidentified noncholinergic vasodilator material.