Mechanism of penile erection in the dog. Pressure-flow study combined with morphological observation of vascular casts.

Abstract

A pressure-flow study of the corpus cavernosum penis in the dog was performed during the flaccid, tumescent, erect and rigid stages. Perfusion was selectively made into the penile deep artery. The erect stage was induced with the local administration of papaverine hydrochloride, and the rigid stage by electrostimulation of the ischiocavernous muscle during the erect stage. Concurrently, vascular casts of the penis at each stage of erection were observed under a scanning electron microscope for the anatomical analysis of the mechanisms controlling cavernous pressure. In the pressure-flow study, it was demonstrated that a combination of decreased arterial resistance and restricted venous outflow was essential to both cause and maintain the erect state. The rigid stage was generated by contraction of the ischiocavernous muscle tightly compressing the crus penis. In the rigid stage, the cavernous pressure was elevated as high as five times the perfusion pressure; nevertheless, no backflow from the cavernous sinus to the deep artery was recognized. By use of the casts, it was confirmed that venous outflow restriction in the erect and rigid stages was due to compression of the postcavernous venules and penetrating veins in the tunica albuginea. The deep artery was occluded in the tunica albuginea in the casts made during the rigid stage, suggesting that the backflow from the corpus cavernosum penis to the deep artery was prevented by this occlusion. Therefore, in the rigid stage, the arterial and venous occlusion isolated the cavernous sinus from the systemic circulation; this mechanism seems to account for the maintenance of the extremely high cavernous pressure.