ANATOMY AND PHYSIOLOGY

Part of “CHAPTER 117 – ERECTILE DYSFUNCTION“

PENILE ANATOMY

Because of its anatomy, the penis has the potential for rapid engorgement with blood, an increase in size, and the development of rigidity. The two corpora cavernosa become engorged with blood during erection (Fig. 117-1). They contain lacunae lined by endothelium possessing contractile elements and have septa that are rich in smooth-muscle cells, elastin, nerves, and small blood vessels.3 The two corpora have a vascular communication and, unlike the corpus spongiosum, are surrounded by a relatively inelastic tunica albuginea. This arrangement enables the generation of very high intracavernosal pressure and rigidity of the penis when venous outflow is reduced and the lacunae are engorged. The glans penis is an extension of the corpus spongiosum.

FIGURE 117-1. Transverse section of the penis. The two corpora caver-nosa become engorged with blood, resulting in penile erection. They are surrounded by the relatively inelastic tunica albuginea, which helps to provide rigidity. (From Clemente CD, ed. Gray’s anatomy, 30th ed. Philadelphia: Lea & Febiger, 1985:1564.)

The arterial supply of the penis derives from the internal pudendal arteries, which are branches of the internal iliac vessels. Each pudendal artery provides a branch to the bulbourethra, a deep artery to one of the corpora cavernosa, and a dorsal artery. Venous blood eventually drains into the deep pelvic veins.

A complex array of autonomic and somatic nerves innervates the penis. Sympathetic fibers originate from thoracolumbar and sacral levels. They reach the pelvic plexus through hypogastric and pudendal nerves. Parasympathetic innervation derives from S2 to S4. The glans penis is rich in nerve endings that convey touch, pain, temperature, and vibration. Although local neural centers in the lumbosacral spinal cord can cause erection in response to stimulation of the penis, penile erections usually are stimulated by olfactory, auditory, visual, and other sensory inputs that are perceived centrally by the frontal, temporal, parietal, or occipital lobes. These areas may be stimulated by memory and fantasy. Signals are sent to the visceral brain, to the rhinencephalon, and subsequently to the centers in the spinal cord.

PHYSIOLOGY OF THE ERECTILE PROCESS

VASCULAR ASPECTS

The normal erectile process requires an increase in blood flow to the corpora cavernosa. Studies have demonstrated that the
direct injection of 20 to 50 mL of saline per minute into the corpus cavernosum of fresh cadavers can initiate an erection. Furthermore, the erection can be maintained by an infusion rate of 12 mL per minute, although infusion into the internal pudendal artery is ineffective.4 Shunting of blood from the deep artery of the cavernosum into the vascular spaces, relaxation of the smooth muscles of the cavernous tissues, and impeded drainage are important factors in the erectile process.5

NEUROMUSCULAR ASPECTS

Histochemical studies indicate that the corpora cavernosa are rich in adrenergic fibers. In vitro studies have demonstrated contractile responses to norepinephrine in the presence of phentolamine, implying β-adrenergic as well as α-adrenergic stimulation.3 The adrenergic nerves are responsible for detumescence. In this respect, endothelin-1, which is present in erectile tissue,6 can, like adrenergic stimulation, increase cytosolic Ca²⁺ and cause smooth muscle contraction. In the corpora cavernosa, acetylcholinesterase-positive fibers are few, and the contraction of the smooth muscle in the presence of high concentrations of acetylcholine is minimal. Interestingly, vasoactive intestinal peptide (VIP), a potent dilator of smooth muscle, is found in the corpora,7 although neither adrenergic nor cholinergic nerves innervate the VIP-containing cells. Levels of VIP in the cavernous spaces of the corpora cavernosa increase during tumescence, and the direct injection of VIP into the corpora cavernosa induces an erection in some normal men and in some men with ED (see Chap. 182 and Chap. 184). Nitric oxide is the primary endothelium-derived relaxing factor,8 and it causes the smooth muscle in the corpora cavernosa to relax. Nitric oxide synthase has been identified in the neurons and endothelium in the corpora cavernosa.9 Nitric oxide synthase and VIP immunoreactivity colocalize to perivascular and trabecular nerve fibers in the corpus cavernosa.10 Importantly, positive staining for nitric oxide synthase is positively correlated with a clinical history of cavernous nerve integrity.11

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