Penile erection is a complex phenomenon that includes coordinated interaction of the nervous, arterial, venous and sinusoidal systems.13 While the neurogenic component to erectile dysfunction after radical prostatectomy is secondary to disruption of the cavernosal nerves,1 the arterial component is thought to arise from the disruption of accessory pudendal arteries or atherosclerosis.25 Breza etal. demonstrated that an accessory pudendal artery supplied additional blood to the penis in seven out of ten cadavers, and because of its close proximity to the prostate and bladder, could easily be compromised during radical pelvic surgery.26 Aboseif et al. showed a 40% incidence of erectile dysfunction after nerve-sparing radical prostatectomy. These patients had a minimal response after surgery to an intracavernosal vasoactive agent despite an adequate response preoperatively.13 This suggests a vascular etiology of postsurgical impotence, which was confirmed with reduced diameter and velocity of penile blood flow via pulsed Doppler ultrasonography.13'27 Polascik and Walsh conferred that arterial insufficiency is a major factor contributing to impotence along with neurovascular bundle disruption.28 However, they identified accessory internal pudendal arteries in only 4% of the patients and could not demonstrate improved sexual function when the accessory pudendal arteries were preserved than when they were sacrificed.28
Intraoperative damage to the neurovascular bundles, which initiate erections, is the main cause of erectile dysfunction after prostatectomy.1 These neurovascular bundles, comprised of cavernous nerves, release nitric oxide in response to sexual stimuli, which initiates a molecular cascade resulting in increased levels of cyclic guanosine monophosphate (cGMP). This cGMP potentiates corporal vasodilatation and smooth muscle relaxation, which ultimately produces an erection.9 Erectile dysfunction occurs immediately after radical prostatectomy secondary to disruption of the neurovascular bundles, and the return of sexual function may take up to 18 months in some individuals.1,20 This varied length of time of return of sexual function may be due to patient age. Younger patients are more likely to have excessive erectile capacity and greater neurovascular regenerative capabilities.21
Another etiology of post-radical prostatecomy erectile dysfunction is the physiologic development of erectile dysfunction in the aging man. The risk of erectile dysfunction is estimated at 26/1000 men annually and increases with age, lower educational status, diabetes, heart disease and hypertension.29 It is not clear as to how much of the erectile dysfunction is secondary to the prostate surgery verus the patients' comorbid conditions.
Helgason etal. found that men with prostate cancer had a significantly greater risk of impaired function in all aspects of sexuality than those without prostate cancer.18 They found the prevalence of physiological impotence to be 31% in the random population, while 71% in the group with prostate cancer. Medications contributing to impotence were diuretics, hydrogen blockers and warfarin.18
Miller et al. examined whether changes in serum hormone levels influenced erectile dysfunction after radical prostatec-tomy.30 They found a statistically significant increase in serum testosterone, free testosterone, estradiol, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as a decrease in dihydrotestosterone (DHT).30 This implies erectile dysfunction after radical prostatectomy can not be explained by androgen deficiency.
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