Vasculogenic and Postoperative Neurogenic Impotence

Normal Erectile and Ejaculatory Function

In the flaccid penis, the sympathetic nervous system keeps the smooth muscle fibers of the corpora cavernosa contracted, thus limiting blood flow to the tissue and the volume of blood present in the penis. When sufficient sexual stimulation is present, the parasympathetic system becomes predominant and an erection is initiated through fibers arising from S2–S4. These fibers travel through the pelvic plexus to reach the cavernous nerves that enter the corpora cavernosa to release the neurotransmitters nitric oxide (NO) and acetylcholine (ACh). The course of the nerves makes them vulnerable to injury during pelvic surgery as they pass closely by the bladder, prostate, and the rectum. Both NO and ACh induce the production of cyclic guanosine monophosphate (cGMP) in the penile smooth muscle tissue, which leads to calcium flux and smooth muscle relaxation. As the smooth muscle surrounding the lacunar spaces of the corpora cavernosa relaxes, a 20- to 40-fold increase in blood flow into the tissue is realized.

The arterial blood supply to the penis is from the common iliac tree, via the internal iliac (hypogastric), internal pudendal, and common penile artery branches. The common penile artery divides into the dorsal penile artery and the deep penile artery. The dorsal artery supplies the skin and glans of the penis, and does not normally contribute blood to the erectile process. Unfortunately, this vessel has been used to measure blood flow to the penis with the archaic penile–brachial index test, giving misleading results. The other branch of the common penile artery is the deep penile artery (cavernosal artery, central penile artery) supplying the corpus cavernosum, and it is the true blood supply for the erectile process.

The penile arteries are small, being approximately 1 to 2 mm in diameter. As blood enters the lacunar spaces and the small blood vessels of the penis, a shear-stress mechanism is initiated in the endothelium, which then produces more NO. This reinforces the process and causes a maximal erection. It is mainly the endothelial NO that maintains blood flow after initiation by neural NO. The increased penile blood volume causes an increase in intracavernosal pressure, and this pressure in turn compresses the small venules leading blood away from the penis, resulting in blood trapping. This veno-occlusive mechanism is crucial in maintaining an erection.

As the erection is terminated, two basic mechanisms come into play. First, the basic sympathetic tone again becomes predominant, which means that smooth muscle tissue in the penis is contracted and blood flow to the penis is reduced. At the same time, cGMP is broken down in the penile tissue by phosphodiesterase 5 (PDE5). The breakdown of cGMP is a continual process occurring throughout the erection. With the reduced blood flow and the lack of neural supply of NO, breakdown now exceeds its production, and this contributes to the contraction of the smooth muscle of the corpora cavernosa. This means that the intracavernosal pressure falls and blood flow is directed away from the penis, which returns to the flaccid state.

With sexual stimulation, the coordination of different stimuli can result in climax and ejaculation. Before ejaculation, smooth muscle contractions transport semen from the epididymis through the vas deferens to the prostatic part of the urethra. This process is called seminal emission and is controlled by sympathetic fibers, which originate in the thoracolumbar part of the spinal cord and run by way of the least splanchnic nerve and the sympathetic chain to the inferior mesenteric ganglion. The postganglionic fibers reach the cavernous nerve through the hypogastric nerve and the pelvic plexus. The dorsal nerve of the penis constitutes the afferent limb of the ejaculatory reflex as it receives sensory input from the glans and carries the signal to the spinal cord at levels S2–S4. Here, somatic fibers traveling through the pudendal nerve are caused to fire, which causes rhythmic contractions of pelvic and periurethral muscles. This results in projectile ejaculation. During ejaculation, sympathetic fibers are responsible for closure of the bladder neck, which prevents retrograde ejaculation into the bladder.

Vasculogenic Erectile Dysfunction

If penile blood flow cannot be increased sufficiently to rapidly fill the penis, ED will result. Such a dysfunction is most often caused by atherosclerotic disease with possible endothelial dysfunction. There is a growing body of evidence linking ED to other cardiovascular disease (CVD) and to the metabolic syndrome. Thus ED and cardiovascular disease have been shown to share risk factors, and ED is widely considered a precursor of more serious vascular disease.

The debut of ED is generally noted to occur 2 to 5 years before other cardiovascular events become evident. This temporal relationship was first noted in the Prostate Cancer Prevention Trial in which men were examined yearly for up to 7 years for both ED and the occurrence of CVD. The prospective study showed that men with ED at study entry had a near-doubling of the rate of cardiovascular events including angina, myocardial infarction, and stroke. Men who had incident ED and who came to the hospital during the follow-up period also showed an increased risk of myocardial infarction or angina when compared to men with persistent normal erectile function. Subsequent studies have reported similar findings.

These observations have led to the view that ED represents the first manifestation of a generalized condition and can be used as a marker of future CVD. This means that the occurrence of ED might present an opportunity for early detection and prevention of further cardiovascular morbidity.