5 research outputs found

    Autonomic control and vascular changes during penile erection in monkeys

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    The mean pressure in the unstimulated corpus cavernosum of monkeys was 12.1 mm Hg. Pelvic nerve stimulation at 8 to 10 Hz produced penile extension and the mean pressure increased to 64.3 mm Hg (47-84% of carotid artery pressure) after a latency of 10 s. On stopping stimulation, recovery to resting levels occurred within 2 min. The response was not blocked by atropine or propranolol. Blood flow through two 19 gauge needles inserted into the corpus cavernosum increased in parallel with the pressure changes, indicating that arterial inflow increased. Stimulation of either hypogastric nerves or the sympathetic chain produced penile retraction but increased corpus cavernosal pressure. The response to pelvic nerve stimulation was partially blocked. It was concluded that both of these nerves contract penile erectile tissue within the corpus cavernosum and constrict arterial inflow

    The physiology of penile erection

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    Erection of the penis results from increase in blood flow into the corpora. The blood flows through the corpus spongiosum and glans which increase in volume, whereas the blood becomes trapped in the corpus cavernosum which becomes rigid as the pressure increases. The protrusion of the penis may be aided by relaxation of the retractor penis muscle. The major erectile fibres lie in the pelvic nerve and anti-erectile fibres in the sacral sympathetic outflow. The hypogastric nerves may contain both nerve types but there is considerable species and individual variation. The neurotransmitters mediating erection have yet to be determined. There is some evidence that acetylcholine is involved in the increase in blood flow through the corpus spongiosum but not in the corpus cavernosum. Vasoactive intestinal peptide may also have a role. It is possible that these and other substances interact to control the complete process. Erection is inhibited by noradrenaline released from sympathetic nerves, and this acts mainly on alpha-1 adrenoceptors within the penis and on the retractor penis muscle. During tumescence blood flows into the sinusoids from the helicine arterioles which supply them. The sinusoids become dilated due to relaxation of smooth muscle within the trabeculae. Blood may also be redirected from anastomoses between the dorsal arteries and corpus spongiosum through other helicine arterioles supplying the sinusoids of the corpus cavernosum. The significance of polsters (smooth muscle projections into the blood vessel lumen) remains controversial. Occlusion of venous drainage from the corpora cavernosa is both passive (due to increased corpus cavernosum pressure) and active. Relaxation of trabecular smooth muscle may also modify blood flow through the corpora cavernosa

    Responses of erectile tissue from impotent men to pharmacological agents

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    Erectile tissue was removed from the corpora cavernosa of 25 impotent men undergoing surgery for insertion of penile prostheses. Strips, set up in an organ bath, were contracted by the alpha-adrenergic agonist phenylephrine. There was no significant difference between tissue taken from men with diabetes, alcoholism, Peyronie's disease or men with no obvious condition causing the impotence. The sensitivity of tissues from hypertensive patients was significantly reduced but this was probably due to drugs being taken for hypertension. Precontracted tissues could be relaxed by acetylcholine or isoprenaline. The responses, however, were inconsistent, so that no difference between the different groups of patients was apparent
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