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Haemodynamics of erection

Created: 21/5/2006
Updated: 21/5/2006


Haemodynamics of erection

Penile erection is a haemodynamic phenomenon resulting from smooth muscle relaxation in the corpus cavernosum and helicine arteries. Erection is characterised by maximal sinusoidal smooth muscle relaxation in the corpora cavernosa, an increase in arterial inflow, and a reduction in venous outflow (due to increased resistance) (see figure 1.0). Vascular smooth muscle relaxation is the primary haemodynamic event underlying each of these three components of the erectile response, and is coordinated through a spinal reflex with central nervous system integration of a variety of sexual stimuli.

Figure 1 Anatomy and mechanism of penile erection. During detumescence inflow in helicine arteries is minimal, with free outflow via the subtunical veins. Relaxation of trabecular smooth muscle and vasodilatation of the arterioles results in increased blood flow and erection.

In the flaccid state, cavernosal smooth muscle is tonically contracted allowing only minimal blood flow for nutritional purposes. It has been estimated that penile arterial inflow increases up to thirty-fold during tumescence. Sexual stimulation (tactile, visual, auditory, olfactory or imaginative) causes an increase in activity in the nerves supplying smooth muscle of the penile arteries and corpus cavernosum, culminating in their relaxation. As a consequence, the compliance of the corpora increases and arterial resistance decreases, exposing the sinusoids to systemic blood pressure and leading to engorgement of blood in the corpus cavernosum. As inflow increases and sinusoidal smooth muscle relaxes, subtunical venules draining the corpus cavernosal tissue become compressed against the inelastic tunica albuginea (see figure 1.1), resulting in veno-occlusion and a rise in intracavernosal pressure. This veno-occlusive mechanism is absent in the corpus spongiosum, which maintains pressure mainly through a high flow state through the glans penis.

Relaxation of corpus cavernosal smooth muscle allows expansion of corpora with accumulation of volume under pressure, enabling the penis to act as a capacitor. In the presence of adequate inflow and high outflow resistance, the capacitor function is limited solely by stiffness of fibroelastic elements of the penis. In general, rigidity is associated with intra-cavernosal pressures of 60-90 mm Hg, although a wide range of pressures have been demonstrated in adequate erections. During the initial phase of erection, both systolic and diastolic flow is increased and continuous. As intracavernosal pressure rises above 40mm Hg, diastolic flow decreases and is reversed at intracavernosal pressures of approximately 80mm Hg. Systolic flow is diminished and flow ceases if intracavernosal pressure approaches systemic blood pressure (or rather systolic occlusion pressure, about 106 mm Hg). Detumescence occurs as a consequence of increased cavernosal smooth muscle tone, contraction of the sinusoids, and a reduction in arterial inflow and venous resistance.

Figure 2

Figure 2
Schematic diagram showing the veno-occlusive mechanism. During flaccidity the helicine arteries are tonically contracted restricting the amount of arterial inflow. With appropriate stimulation vascular smooth muscle relaxation leads to an increase in arterial inflow. As the sinusoidal spaces fill with blood the subtunical venules become compressed by the inelastic tunica albuginea, cavernosal pressure increases and tumescence ensues.

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