Male Sexual Function (part 2)
Vascular changes at erection
Erection is a phenomenon produced by arterial vasodilatation associated with smooth muscle relaxation of the corpora. This enables blood to flow into the dilated cavernous spaces. Recent evidence suggests that venous resistance also increases to retain blood in the corpora. The rise in venous resistance is probably a consequence of external compression by the engorged corpora rather than vasoconstriction. Many theories have been advanced over the years on the existence of vascular shunts that divert blood into the corpora at erection and conversely open to empty blood at detumescence. There is no reliable evidence to support this concept, and simple dilatation of the arterial supply to the penis and the trabeculae of the corpora is adequate to explain the vascular mechanism involved in erection.
Neural control of erection
Erection can be produced in response to psychogenic stimuli arising in the cerebral cortex (fantasy) as well as visual and auditory sensory stimulation. These stimuli descend from the higher centres to the spinal cord. Alternatively, tactile stimulation of the penis can produce erection via a reflex arc that sends impulses through sacral segments of the spinal cord without ascending to the brain. The parasympathetic supply appears to be the most important neurological control mechanism for erection. Physiological information from animal experiments has provided some data, but observations in men with spinal cord injury provide the most reliable information in humans.
Lesions of the sacral cord segments abolish the sacral spinal reflex arc and the penis does not respond to tactile genital stimulation. Erections may, however, still be produced by psychogenic stimuli such as erotic material and fantasy. This is mediated by pathways linking the cerebral cortex to the thoracolumbar cord sympathetic outflow from T10 to T12. Conversely, less than 10% of patients with lesions above T12 can achieve erection in response to pyschogenic stimuli. This increases to over 50% in patients with lumbar lesions.
Emission and ejaculation
As previously explained, the cauda of the epididymis acts as a sperm reservoir. The muscle fibres around the cauda epididymis and vas contract during the ejaculation process. Emission involves the deposition of seminal fluid into the posterior urethra. At the same time, the bladder neck closes to prevent retrograde passage of semen into the bladder. Contraction of the vas deferens during emission and closure of the bladder neck are under the control of sympathetic nerve fibres. These same fibres innervate the prostate and seminal vesicles, which produce nearly all of the seminal fluid.
Factors interfering with the function of these nerve fibres can, therefore, lead to a number of complaints, including retrograde ejaculation (caused by failure of closure of the bladder neck) or aspermia (absence of semen or ‘dry orgasm’.) These factors include trauma to the the pelvic nerve plexus and treatment with a-adrenergic-blocking agents, which interfere with the action of noradrenaline released from sympathetic nerve terminals. Ejaculation is the process leading to the expulsion of semen from the posterior urethra via the urethral meatus as a consequence of contractions of the striated perineal muscles. These are innervated by the pudendal nerve, which is somatic in origin.
