Arterial surgery for erectile dysfunction

Abstract

A normal human erection is dependent upon an intact neuroendocrine system, adequate arterial blood flow, compliance of sinusoidal tissue within the corpora, and an intact veno-occlusive mechanism. A normal endocrine milieu with adequate levels of circulating androgens and low levels of prolactin appears to be important for normal erectile function. During the flaccid state of the penis the smooth muscles lining the sinusoidal spaces and the arteries are tonically contracted. The primary event in the production of a human erection appears to be non-adrenergic, non-cholinergic(NANC) stimulation of vascular endothelium synthesis of NO, which causes smooth muscle relaxation of the sinusoidal tissue within the corpora and penile arteries. Blood flow into the corpora increases dramatically and the sinusoids expand as they fill with blood. During the early filling stage the venous drainage of the corpora is unimpeded. As the sinusoids expand, the emissary veins are compressed on the underside of the tunica albuginea and passively occluded. During the latter portion of the filling phase, the penis becomes engorged and eventually becomes rigid as intracorporeal pressure reaches and exceeds mean arterial blood pressure. Patients with impaired arterial blood flow but a normal veno-occlusive mechanism will take longer to fill but may be able to achieve adequate rigidity. During a full erection, the arterial blood flow is reduced but still higher than during the flaccid state. Intracorporeal pressures are transiently higher than arterial blood pressure due to bulbocavernosus muscle contraction around the corpora. Orgasm and ejaculation are accompanied by adrenergic release which is the stimulation of detumescence. Release of alphaadrenergic neurotransmitters during ejaculation stimulates vascular smooth muscle contraction within the corpora. Experimental studies have shown that the norepinephrine is responsible for detumescence. This is why alpha agents such as phenylephrine are so effective at reversing the effects of pharmacologically stimulated erections. In addition, endogenous catecholamines released by the adrenals in response to anxiety can interfere with a patient’s response to pharmacologically stimulated erection. Thus anxiety, ‘clinic effect’, can produce artifactual results during assessment of the vascular system.