Physiology of Penile Erection and Pathophysiology of Erectile Dysfunction
The molecular and clinical understanding of erectile function continues to gain ground at a particularly fast rate. Advances in gene discovery have aided greatly in working knowledge of smooth muscle relaxation/contraction pathways. Intensive research has yielded many advances. The understanding of the nitric oxide pathway has aided not only in the molecular understanding of the tumescence but also aided greatly in the therapy of erectile dysfunction. As a man ages or undergoes surgery, preventative therapies to preserve erectile dysfunction have begun. All clinical interventions derived their beginning in a full anatomical, molecular, and dynamic knowledge base of erectile function and dysfunction. In this chapter the components of erectile function will be explained.
Hemodynamics and Mechanism of Erection and Detumescence
The penile erectile tissue, specifically the cavernous smooth musculature and the smooth muscles of the arteriolar and arterial walls, plays a key role in the erectile process. In the flaccid state, these smooth muscles are tonically contracted, allowing only a small amount of arterial flow for nutritional purposes. The blood partial pressure of oxygen (PO2) is about 35mmHg range. 1 The flaccid penis is in a moderate state of contraction, as evidenced by further shrinkage in cold weather and after phenylephrine injection.
Sexual stimulation triggers release of neurotransmitters from the cavernous nerve terminals. This results in relaxation of these smooth muscles and the following events:
Dilatation of the arterioles and arteries by increased blood flow in both the diastolic and the systolic phases
Trapping of the incoming blood by the expanding sinusoids
Compression of the subtunical venular plexuses between the tunica albuginea and the peripheral sinusoids, reducing the venous outflow
Stretching of the tunica to its capacity, which occludes the emissary veins between the inner circular and the outer longitudinal layers and further decreases the venous outflow to a minimum
An increase in PO2 (to about 90 mmHg) and intracavernous pressure (around 100 mm Hg), which raises the penis from the dependent position to the erect state (the full-erection phase)
A further pressure increase (to several hundred millimeters of mercury) with contraction of the ischiocavernosus muscles (rigid-erection phase)
The angle of the erect penis is determined by its size and its attachment to the puboischial rami (the crura) and the anterior surface of the pubic bone (the suspensory and funiform ligaments). In men with a long heavy penis or a loose suspensory ligament, the angle usually will not be greater than 90 degrees, even with full rigidity.