ERECTION AND EJACULATION

Erection is purely vascular. It occurs in response to parasympathetic stimulation and is independent of compression by the ischiocavernosi and bulbospongiosus, although these may contribute to maximum rigidity. Sexual arousal leads to rapid inflow from the helicine arteries following relaxation of the smooth muscle of the corpora cavernosa, an event which is dependent on the production of nitrous oxide and cyclic GMP. This inflow of blood fills the cavernous spaces leading to tumescence. The resulting distension converts tumescence to erection by pressure on the subtunical veins, which drain the erectile tissue, thereby obstructing them. The pressure within the corpora cavernosa is maintained at 100 mmHg to maintain penile erection. Continuing cutaneous stimulation of the glans and frenulum contributes significantly to maintaining erection and initiating orgasm and ejaculation. Erection is thus dependent on a normal psychogenic response to stimulation, intact parasympathetic nerves, corporal smooth muscle capable of relaxation, patent arteries capable of delivering blood at the required rate, and a normal venous system.

Ejaculation consists of two processes: emission and ejaculation. Emission is the transmission of seminal fluid from the vasa, prostate and seminal vesicles into the prostatic urethra under sympathetic control. Ejaculation is the onward transmission of seminal fluid from the prostatic urethra to the exterior. This has autonomic and somatic components. The first discernible part of the process is contraction of bulbospongiosus, which contracts about six times under somatic control. The way in which seminal fluid crosses the external urethral sphincter into the bulbar urethra is not clear: it is known to be under autonomic control and is timed such that from the second to the final contraction of bulbospongiosus the ejaculate appears from the external meatus, in some younger men in a pulsatile fashion.
Failure to achieve tumescence with adequate stimulation is termed impotence or more recently and politically correctly, erectile dysfunction. The mechanism of erection is complex: failure in any of the previously mentioned components can result in impotence. The commonest causes include psychogenic disturbance with failure to relax cavernous smooth muscle; arterial insufficiency, as a result of atheromatous disease; and damage to the parasympathetic nervous system secondary to diabetes or following pelvic surgery such as radical prostatectomy, radical cystectomy or bowel resection. Pharmacotherapy is predominantly directed at achieving cavernosal smooth muscle relaxation.
Detumescence is effected through the sympathetic pathway. Failure of an erection to detumesce is termed priapism. This can occur spontaneously but is most commonly seen with conditions that impair blood flow by increasing its viscosity such as sickle cell anaemia or leukaemia, or as a consequence of drug treatment when given by injection. These conditions result in ischaemia of the corporal smooth muscle, which causes pain within the penis.
Peyronie's disease produces a bend in the erect penis. This is most commonly a dorsal curvature and results from a localized thickening or plaque of the corpora cavernosa which prevents expansion of a segment during erection.

REFERENCES

Lepor H, Gregerman M, Crosby R, Mostofi FK, Walsh PC 1985 Precise localization of the autonomic nerves of the pelvic plexus to the corpora cavernosa: a detailed anatomical study of the adult male pelvis. J Urol 133: 207-212. Medline Similar articles
Mundy AR, Fitzpatrick J, Neal D, George N (eds) 1999 Male sexual function. In: The Scientific Basis of Urology, Chapter 12. Isis Medical Media: 243-53.
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