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Penile microarterial bypass surgery (MABS) may be the only treatment capable of restoring normal erectile function without the necessity for the chronic use of vasoactive medications or placement of a penile prosthesis. Lack of standardization in patient selection, hemodynamic evaluation, surgical technique, and limited long-term outcome data using validated instruments has resulted in this surgery being considered experimental. The members of the Erectile Dysfunction Guideline Update Panel reviewed the available MABS publications and only four of 31 manuscripts met the criteria for the Arterial Occlusive Disease Index patient. The total studied population of these four publications was 50, which was considered too small to determine if MABS is effective or not. Reported successful outcomes were 36-80 and 91% for inferior epigastric artery (IEA) to dorsal vein and IEA to dorsal artery MABS, respectively. We recently published the largest long-term outcome MABS study using validated questionnaires (71 men aged 30.5 +/- 9.2 years; mean follow-up 34.5 +/- 18 months). The mean pre- and postoperative total International Index of Erectile Function, erectile function domain, questions 3 and 4 scores were 35.5 +/- 14.8, 13.7 +/- 6.7, 2.2 +/- 1.4, 2.1 +/- 1.3, and 56.2 +/- 16.6, 23.8 +/- 6.6, 4.1 +/- 1.4, and 3.9 +/- 1.5, respectively. In addition, 55 and 73% of patients reported erectile function domain scores > or =26 and 21, respectively, and almost 90% of patients would recommend or undergo MABS again. In addition, changes in pre- and postoperative sexual distress scale scores and the Center for Epidemiologic Studies Depression Scale were statistically significant. More importantly, treatment satisfaction (EDITS) was very high, and 87% of patients would recommend the surgery to someone else and 88.7% reported a significant improvement in their erectile function. In patients with no vascular risk factors and pure cavernosal arterial insufficiency, MABS provides long-term improvements in erectile function, depression, and overall satisfaction.

Introduction: Pharmacotherapy is the usual initial therapy for most men with erectile dysfunction., Aim: To review the current data relating to the efficacy, tolerability and safety of drugs used in the treatment of men with erectile dysfunction., Methods: A critical review of the literature relating to the use of pharmacotherapeutic agents was undertaken by a committee of eight experts from five countries, building on prior reviews., Main Outcome Measures: Expert opinion and recommendations were based on grading of evidence-based literature, internal committee dialogue, open presentation, and debate., Results: Almost all currently available evidence relates to sildenafil, tadalafil, and vardenafil. Phosphodiesterase type 5 (PDE5) inhibitors are first-line therapy for most men with erectile dysfunction who do not have a specific contraindication to their use. There is no evidence of significant differences in efficacy, safety, and tolerability between the PDE5 inhibitors and apomorphine. Intracavernosal injection therapy with alprostadil should be offered to patients as second line therapy for erectile dysfunction. Intraurethral alprostadil is a less effective treatment than intracavernosal alprostadil for the treatment of men with erectile dysfunction., Conclusions: PDE5 inhibitors are effective, safe, and well-tolerated therapies for the treatment of men with erectile dysfunction. Apomorphine, intracavernosal injection therapy with alprostadil, and intraurethral alprostadil are all effective and well-tolerated treatments for men with erectile dysfunction. We recommend some standardization of the assessment of psychosocial outcomes within clinical trials in the field of erectile dysfunction.

Purpose: Penile microarterial bypass surgery may be the only treatment capable of restoring normal erectile function without the necessity of chronic use of vasoactive medications or placement of a penile prosthesis. Lack of standardization in patient selection, hemodynamic evaluation, surgical technique and limited long-term outcome data using validated instruments have resulted in this surgery being considered experimental. In this study we report long-term outcome data using validated questionnaires in young men (younger than 55 years) free of vascular risk factors who underwent microvascular arterial bypass surgery., Materials and Methods: This is a single institution retrospective institutional review board approved study of 71 men (mean age 30.5 +/- 9.2 years) who underwent microvascular arterial bypass surgery between 1996 and 2007 (mean followup 34.5 +/- 18 months)., Results: Mean preoperative and postoperative penile rigidity measures with and without phosphodiesterase type 5 inhibitors were 41%, 77% and 71%, 90.8%, respectively. Mean total International Index of Erectile Function score, Erectile Function domain, and question 3 and 4 scores preoperatively and postoperatively were 35.5 +/- 14.8, 13.7 +/- 6.7, 2.2 +/- 1.4 and 2.1 +/- 1.3, and 56.2 +/- 16.6, 23.8 +/- 6.6, 4.1 +/- 1.4 and 3.9 +/- 1.5, respectively. Preoperative and postoperative Center for Epidemiologic Studies Depression Scale scores were 42.0 +/- 10.0 and 33.7 +/- 6.1. Treatment satisfaction according to the Erectile Dysfunction Inventory of Treatment Satisfaction was high. All differences were statistically significant. Short-term complications included emesis (2 of 71), dysuria (5 of 71) and wound infection (2 of 71). Long-term complications were loss of penile length (20 of 71) and decreased penile sensation (18 of 71). There were no cases of prolonged penile pain or glans hyperemia., Conclusions: In patients with no vascular risk factors and pure cavernous arterial insufficiency, microvascular arterial bypass surgery provides long-term improvements in erectile function, depression and overall satisfaction.

Objective: To report the experience of three highly specialized centres in the vascular evaluation of erectile dysfunction (ED) in teenagers, as there is little information on this topic, and although clinical guidelines support the use of vascular studies in selected cases, our experience is that vascular evaluation aimed at diagnosing organic ED is uncommon in teenagers, and most are designated as having psychogenic ED., Patients and Methods: In a retrospective multi-institutional analysis of three ED databases (1998-2003) we assessed males aged < or =19 years presenting with ED. The review of these databases focused on demographic characteristics, risk factors for ED, erectile function, results of vascular evaluation, and the causes of ED., Results: In all, 40 males aged 14-19 years were identified. The mean (range) duration of ED at presentation was 22.6 (4-84) months. The major risk factors for ED were antecedent perineal trauma (37%) and penile trauma or surgery (15%). The mean (sd) International Index of Erectile Function 'erectile function' domain score was 15 (4). Information obtained by history taking was not predictive of the cause of ED. Vascular studies were performed in 62% of the patients and 48% of these patients were found to have an underlying vascular pathology; 42% of the latter group were found to be possible candidates for surgical intervention and another 16% needed further angiographic evaluation., Conclusion: ED in teenagers should not be routinely categorized as psychogenic without an adequate vascular evaluation, as a significant percentage have abnormal erectile haemodynamics consistent with vasculogenic ED.

Introduction: Is cavernosometry a useful tool in treating men with erectile dysfunction?, Methods: Five people with expertise and/or interest in the area of cavernosometry were asked to contribute their opinions., Main Outcome Measure: To provide food for thought, discussion, and possible further research in a poorly discussed area of sexual medicine., Results: While one urologist feels dynamic infusion cavernosography and cavernosometry seem to have found their place in history, another believes it is time to separate these tests and look at cavernosometry alone and its relevance to the use of duplex Doppler ultrasound, both useful tools in assessing surgical candidates. Three clinicians agree that cavernosography and cavernosometry have a role in specific cases, particularly before revascularization surgery., Conclusion: Cavernosometry may not be a useful tool for the average clinician treating erectile dysfunction, but serves a purpose for the specialist.

Introduction: Ischemic priapism is associated with cavernosal acidosis, which decreases the efficacy of adrenergic agonists. We determined the effect of acidosis on ligand dissociation from adrenergic receptors and assessed the efficacy of high-dose phenylephrine in treating patients with acute ischemic priapism., Methods: Dissociation rates of [3H]prazosin were determined at pH 7.2 and 6.9 in membrane preparations of rabbit penile cavernosal tissue. Vital signs were recorded from patients before injection, and at 1 minute and 5 minutes after injection of high-dose phenylephrine (1,000 mg q 5 minutes) for 17 consecutive cases of iatrogenic ischemic priapism that occurred after vascular assessment. We also provide two case reports of prolonged ischemic priapism successfully managed with high-dose phenylephrine., Results: Dissociation rates of [3H]prazosin were greater at pH 6.9 (K (-1) = 0.23/minute) than at pH 7.2 (K (-1) = 0.10/minute), suggesting decreased receptor affinity at acidic pH. Intracavernosal therapy with high-dose phenylephrine (mean dose 2,059 +/- 807 microg) was 100% effective with no adverse events or significant changes in vital signs. In addition, two patients with ischemic priapism for > or =36 hours were successfully treated with high-dose intracavernosal phenylephrine (mean dose 45,000 microg) without any adverse event. Both patients are currently potent., Conclusions: Acidic pH may decrease the binding affinity of adrenergic ligands to their receptors. Phenylephrine at doses higher than previously reported may be necessary to overcome this decreased affinity in acidosis associated with ischemic priapism. High-dose intracavernosal phenylephrine administration is safe and effective in the management of ischemic priapism. Continuous cardiovascular monitoring is advised.

Background: Diabetes is associated with declining sexual function in women. However, the effects of diabetes on genital tissue structure, innervation and function remains poorly characterized. In control and streptozotocin-treated female rats, we investigated the effects of diabetes on vaginal blood flow, tissue morphology, and expression of arginase I, endothelial nitric oxide synthase (eNOS) and cGMP-dependent protein kinase (PKG), key enzymes that regulate smooth muscle relaxation. We further related these changes with estrogen receptor alpha (ERalpha) and androgen receptor (AR) expression., Results: In addition to significantly elevated blood glucose levels, diabetic rats had decreased mean body weight, lower levels of plasma estradiol, and higher plasma testosterone concentration, compared to age-matched controls. Eight weeks after administration of buffer (control) or 65 mg/kg of streptozotocin (diabetic), the vaginal blood flow response to pelvic nerve stimulation was significantly reduced in diabetic rats. Histological examination of vaginal tissue from diabetic animals showed reduced epithelial thickness and atrophy of the muscularis layer. Diabetic animals also had reduced vaginal levels of eNOS and arginase I, but elevated levels of PKG, as assessed by Western blot analyses. These alterations were accompanied by a reduction in both ERalpha and AR in nuclear extracts of vaginal tissue from diabetic animals., Conclusion: In ovariectomized (estrogen deficient) animals, previous reports from our lab and others have documented changes in blood flow, tissue structure, ERalpha, arginase I and eNOS that parallel those observed in diabetic rats. We hypothesize that diabetes may lead to multiple disruptions in sex steroid hormone synthesis, metabolism and action. These pathological events may cause dramatic changes in tissue structure and key enzymes that regulate cell growth and smooth muscle contractility, ultimately affecting the genital response during sexual arousal.

Introduction: Oral contraceptives (OCs) have been the preferred method of birth control because of their high rate of effectiveness. OC use, however, has been associated with women's sexual health complaints and androgen insufficiency. OC use is associated with a decrease of androgen ovarian synthesis and an increase in the production of sex hormone-binding globulin (SHBG). There have been limited studies assessing SHBG values after discontinuation of OC use., Aim: To retrospectively investigate SHBG levels before and after discontinuation of OC use., Main Outcome Measure: Sex hormone-binding globulin values were compared at baseline, while on the OC, and well beyond the 7-day half-life of SHBG at 49-120 (mean 80) days and >120 (mean 196) days after discontinuation of OCs., Methods: A total of 124 premenopausal women with sexual health complaints for >6 months met inclusion/exclusion criteria. Three groups of women were defined: (i) "Continued-Users" (N = 62; mean age 32 years) had been on OCs for >6 months and continued taking them; (ii) "Discontinued-Users" (N = 39; mean age 33 years) had been on OCs for >6 months and discontinued them; and (iii) "Never-Users" (N = 23; mean age 36 years) had never taken OCs., Results: Sex hormone-binding globulin values in the "Continued-Users" were four times higher than those in the "Never-User" group (mean 157 +/- 13 nmol/L vs. 41 +/- 4 nmol/L; P < 0.0001). Despite a decrease in SHBG values after discontinuation of OC use, SHBG levels in "Discontinued-Users" remained elevated in comparison with "Never-Users" (N = 26; P < 0.0001 for >120 days)., Conclusion: In women with sexual dysfunction, SHBG changes in "Discontinued-Users" did not decrease to values consistent with "Never-Users." Long-term sexual, metabolic, and mental health consequences might result as a consequence of chronic SHBG elevation. Does prolonged exposure to the synthetic estrogens of OCs induce gene imprinting and increased gene expression of SHBG in the liver in some women? Prospective research is needed.

Introduction: From 1999 to 2004, there had been 21 publications from multiple medical specialties (sexual medicine, urology, neurology, cardiology, biomedical engineering, sports medicine, emergency medicine, and officials from the National Institute for Safety and Occupational Health) investigating the relationship between bicycle riding and erectile dysfunction (ED). In the previous 18 years, there have been 14 such studies., Aim: The primary aim was to summarize accumulating data on the safety of bicycle riding based on medical evidence categorized by levels of evidence, including case reports, observational studies, case control studies, mechanistic studies, and population-based epidemiologic investigations. The secondary aim was to address the concerns of bicyclists and propose measures to minimize the risk of ED associated with bicycle riding., Methods: An English-language medical literature review was made of publications in peer review journals from 1981 to 2004, including published abstract presentations at major medical meetings., Main Outcome Measure: Ranked published epidemiologic data on bicycle riding and ED., Results: Bicycle riding more than 3 hours per week was an independent relative risk (RR = 1.72) for moderate to severe ED. In case control studies, the prevalence of moderate to severe ED in bicyclists was 4.2% and 4% vs. age-matched runners 1.1% (P < or = 0.018) and swimmers 2% (P = 0.05), respectively. Therefore, bicycle riders should take precautionary measures to minimize the risk of ED associated with bicycle riding: change the bicycle saddle with a protruding nose to a noseless seat, change the posture to a more upright/reclining position, change the material of the saddle (GEL), and tilt the saddle/seat downwards., Conclusions: The mechanism is hypothetically related to the rider interaction with the bicycle saddle at the perineum-saddle interface. Straddling bicycle saddles with a nose extension is associated with suprasystolic perineal compression pressures, temporarily occluding penile perfusion and potentially inducing endothelial injury and vasculogenic ED.

Purpose: To investigate the differential impact of straddles (A(ns) and B(ns)) and noseless two-cheek seats (A(ntcs) and B(ntcs)) on penile hemodynamics and perineal compressive forces in subjects who cycle in a stationary bicycle., Materials and Methods: Subjects underwent cavernosal artery peak systolic velocity (CAPSV) measurements after intracavernosal injection of vasoactive agents while supine, sitting upright on an examination table, straddling a saddle, sitting on a seat, and again supine. Mean perineal compression pressures recorded while straddling the saddles were compared with those while sitting upright., Results: No differences were found in right and left CAPSV values while supine, sitting upright on an examination table, sitting on a seat, and supine again. Right/left CAPSV (cm/second) values straddling A(ns) and saddle B(ns) (0.7 +/- 2.9/1.5 +/- 6.2 and 0/0, respectively) were significantly lower than values obtained while sitting on A(ntcs) and B(ntcs) (25.6 +/- 13.4/23.8 +/- 12.0 and 17.3 +/- 6.4/18.3 +/- 6.5, respectively) (P < 0.001). Mean perineal compression pressures (mm Hg) on A(ns) and saddle B(ns) (315.2 +/- 39 and 387.9 +/- 64.3, respectively) were significantly higher than values obtained while sitting upright on an examination table (47.6 +/- 5.2 and 46.0 +/- 8.1, respectively) (P < 0.001)., Conclusions: We have identified an objective test to assess if an individual bicycle rider, sitting on a certain shape of bicycle saddle or seat generates sufficient compressive forces at the perineal-saddle interface to obstruct cavernosal arterial inflow. This study also demonstrated that straddling bicycle saddles with nose extensions is associated with perineum-saddle interface compressive pressures that exceed systolic perfusion pressures, significantly diminishing penile hemodynamics.

Objective: To report gray scale, volumetric, and duplex ultrasound data before and after sexual stimulation in a large population of women with sexual dysfunction., Design: Retrospective review of women with sexual dysfunction., Setting: An academic center., Patient(s): Pre- and postmenopausal women with sexual dysfunction., Intervention(s): None., Main Outcome Measure(s): This is an Institutional Review Board-approved retrospective study of 142 women who underwent duplex Doppler ultrasound (DDU) arousal testing for sexual dysfunction., Result(s): This study revealed that DDU was able to record morphologic, volumetric (clitoral and corpora spongiosa diameters), and hemodynamic (peak systolic and end-diastolic) changes in women with sexual dysfunction before and after sexual stimulation. Resistive index measurements, which are indicative of veno-occlusive function, did not significantly change before and after arousal in both the clitoris and corpora spongiosa. We also found a correlation between genital diameter and genital end-diastolic velocity value. Gray scale scanning revealed tunical thickening or plaque in several patients who sustained blunt perineal trauma., Conclusion(s): The role of DDU in the management of women with sexual dysfunction remains to be determined; however, end-diastolic velocity values suggest that this parameter has an important physiologic implication as a direct determinant of genital engorgement.

Objectives: To describe the urologic and sexual complications of male survivors of sexual torture, including prevalence, sequelae, diagnosis, and treatment., Methods: Through chart reviews, we identified all male survivors of torture who had been treated for physical and/or psychological symptoms due to sexual trauma at the Boston Center for Refugee Health and Human Rights at Boston Medical Center between January 1, 2001 and January 1, 2002. Of the 72 men seen, 20 (28%) were survivors of sexual trauma. Our study focused on genital trauma leading to urologic and/or sexual dysfunction. Therefore, all cases of male genital trauma that had been referred to the urology department (3 of 20) were selected for this review., Results: The patients presented with chronic genital and erectile pain, lower urinary tract symptoms, and sexual dysfunction. The diagnostic workup included history, physical examination, and ultrasonography. Treatment included steroid injections for chronic pain and oral erectogenic agents for sexual dysfunction., Conclusions: The apparent prevalence and severity of the physical and mental sequelae to sexual trauma make it an important area for screening when treating survivors of torture. Our study is the first of its kind to document urologic complications of sexual torture in a foreign-born U.S. cohort of tortured men, including prevalence, diagnosis, and treatment. The proposed use of steroid injections in the clinical treatment of these patients has not been previously reported.

Purpose: The effects of subphysiological and physiological levels of estradiol on vaginal blood flow and estrogen receptor were investigated., Materials and Methods: Intact or ovariectomized female Sprague-Dawley rats were used. Two weeks after surgery rats were infused with vehicle (polyethyleneglycol), or estradiol at subphysiological (5 microg daily) or physiological (15 microg daily) concentrations for 14 days using osmotic pumps. Changes in vaginal blood flow elicited by pelvic nerve stimulation were assessed by laser Doppler flowmetry. Total levels of functional estrogen receptor were determined by radioligand binding and Western blot analyses were used to assess estrogen receptor (ER) alpha protein., Results: Mean plasma estradiol concentration +/- SEM decreased by 63% in the vehicle group (intact 36.5 +/- 10.3 pg/ml). The subphysiological and physiological estradiol groups had plasma levels that were 55% and 83% of the intact group, respectively. Uterine and vaginal wet weight, and vaginal blood flow were significantly decreased in the vehicle group and normalized by physiological levels of estradiol. However, vaginal blood flow was significantly greater in the subphysiological estradiol group compared to intact animals. Specific binding of [H]estradiol in vaginal tissue extracts from intact rats was 0.51 fmol/mg protein and it was increased 30-fold in the vehicle group. ER binding in vaginal tissue in the physiological estradiol group decreased to levels that were comparable to those in intact animals, whereas estrogen receptor binding remained elevated in the subphysiological estradiol group. These changes were paralleled by ERalpha protein levels., Conclusions: Estradiol is crucial for maintaining optimal vaginal blood flow in the rat. Lower levels of plasma estradiol trigger compensatory ERalpha up-regulation.

A 58-year-old man presented with a 6-month history of painful progressive penile firmness, initially diagnosed as Peyronie's disease. Penile fibrosis involved the entire corpora cavernosa and spongiosum, making it consistent with three-chamber priapism. Cavernosal biopsies revealed epithelioid hemangioendothelioma, and the metastatic workup found hepatic and pulmonary lesions. The patient was treated with paclitaxel, but eventually died of cancer progression. Early infiltrative vascular malignancies of the penis may be indistinguishable from Peyronie's disease. A review of published reports revealed that penile masses associated with progressive growth, obstructive urinary symptoms, dysuria, or painful erections might warrant further evaluation with biopsies.

Purpose: We established a rat model to investigate the female vaginal arousal response and the role of the nitric oxide (NO) pathway on vaginal blood flow in vivo., Materials and Methods: Vaginal blood flow changes induced by pelvic nerve stimulation (PNS) in female Sprague-Dawley rats were determined by laser Doppler flowmetry. Frequency response data were determined in each animal. In addition, changes in vaginal blood flow were measured after intravenous administration of the NO synthase inhibitor L-NAME (NG-nitro-L-arginine methyl ester) or the phosphodiesterase type 5 inhibitor sildenafil in response to PNS at submaximal frequency. Changes in blood flow were evaluated by comparing the area under the curve of each response., Results: Reproducible frequency dependent increases in vaginal blood flow were observed in response to PNS. Administration of L-NAME (a NO synthase inhibitor) resulted in significant attenuation (25.6% to 18.2% vs control at 30 minutes, p <0.00001) of the PNS induced increase in vaginal blood flow. In contrast, sildenafil administration significantly increased PNS induced vaginal blood flow (166.9% +/- 25.8% vs control at 30 minutes, p <0.00001)., Conclusions: Our data suggest that the rat is a useful and reliable animal model for investigating the vaginal arousal response. In addition, we used this model to demonstrate the important role of the NO-cyclic guanosine monophosphate pathway in vaginal arousal.

In this study, we investigated the binding characteristics of [3H]Delta(5)-androstene-3beta,17beta-diol to rabbit vaginal cytosolic and nuclear extracts and in freshly excised intact tissue strips. [3H]delta(5)-Androstene-3beta,17beta-diol bound to a protein(s) in the vaginal nuclear extract with high affinity (K(d)=3-5 nM) and limited capacity (50-100 fmol/mg protein). No specific binding was detected in the cytoplasmic extracts. Competitive binding studies showed that binding of [3H]delta(5)-androstene-3beta,17beta-diol was effectively displaced with unlabeled delta(5)-androstene-3beta,17beta-diol but not with dehydroepiandrosterone, testosterone, dihydrotestosterone, triamcinolone acetonide, or progesterone. However, estradiol at high concentrations partially displaced bound [3H]delta(5)-androstene-3beta,17beta-diol. Incubation of freshly excised vaginal tissue strips with [3H]delta(5)-androstene-3beta,17beta-diol in the absence or presence of excess unlabeled delta(5)-androstene-3beta,17beta-diol for 1h at 37 degrees C resulted in specific binding to a soluble macromolecule in the nuclear KCl extracts. In addition, quantitative measurement of estrogen receptor, androgen receptor and delta(5)-androstene-3beta,17beta-diol binding protein was performed by equilibrium ligand binding assays using extracts of distal vaginal tissue from intact animals or ovariectomized animals treated for 2 weeks with vehicle, estradiol, testosterone, or estradiol plus testosterone. These changes in steroid hormone levels resulted in opposing trends between the estrogen receptor and delta(5)-androstene-3beta,17beta-diol binding protein, suggesting that delta(5)-androstene-3beta,17beta-diol binding protein is regulated differently by the hormonal milieu than the estrogen receptor. These data suggest that rabbit vaginal tissue expresses a novel binding protein which specifically binds delta(5)-androstene-3beta,17beta-diol and is distinct from the androgen and estrogen receptors.

Objectives: To assess the physiologic and biochemical changes resulting from ischemia and reperfusion. Effective therapy for ischemic priapism reestablishes corporal venous outflow and arterial inflow and results in increased corporal partial pressure of oxygen. Data are limited concerning reperfusion injury of ischemic erectile tissue associated with reactive oxygen species (ROS) and the potential role of ROS scavengers in the clinical therapy of ischemic priapism., Methods: Anesthetized adult New Zealand white male rabbits (n = 7) were exposed to a low oxygen tension breathing gas to achieve hypoxia within the corpora cavernosa. This resulted in a mean systemic oxygen saturation of 60%. The pelvic nerve was electrically stimulated to induce penile erection, and the base of the erect penis was clamped. After varying durations of ischemia, the clamp was removed to allow reperfusion. We determined the intracavernosal oxygen tension, histologic changes, myeloperoxidase activity, and lipid peroxidation., Results: Corporal partial pressure of oxygen progressively decreased as the duration of priapism increased. A statistically significant increase was noted in myeloperoxidase activity and lipid peroxidation with corporal reperfusion. Polymorphonuclear leukocyte infiltration was documented in the ischemic reperfused tissue., Conclusions: In the management of ischemic priapism, reperfusion causes erectile tissue injury owing to the presence of ROS. There is a need to investigate the utility of ROS scavengers and antioxidants in the management of ischemic priapism.

Purpose: We review contemporary scientific data concerning the physiology and pharmacology of peripheral female genital arousal responses in the animal (rabbit and rat) model., Materials and Methods: We reviewed the contemporary literature and our research studies concerning physiology and pharmacology of peripheral genital arousal from 3 experimental animal models, including genital smooth muscle cell culture, genital strip organ bath and in vivo animal model studies., Results: Nitric oxide (NO) appears to be a key pathway mediating clitoral smooth muscle relaxation. In the vagina NO appeared to have a more controversial role in mediating vaginal muscularis smooth muscle relaxation. Vasoactive intestinal polypeptide induced vaginal smooth muscle relaxation. Functional alpha-adrenergic receptors were expressed in the clitoris and vagina, and mediated norepinephrine induced genital smooth muscle contraction. Androgens and estrogens modulated distinct physiological responses in vagina, and androgens facilitated vaginal smooth muscle relaxation. Papaverine hydrochloride, a smooth muscle relaxant, and phentolamine mesylate, an alpha-blocker, administered into the vaginal spongy muscularis layer increased vaginal wall pressure and vaginal blood flow. Sildenafil caused significant increases in genital (clitoral and vaginal) blood flow and vaginal lubrication in intact and ovariectomized animals. This response was more pronounced in animals treated with estradiol, suggesting that the NO cyclic guanosine monophosphate pathway is involved in the physiological mechanism of female genital arousal and that sildenafil facilitates this response in an in vivo animal model., Conclusions: To achieve improved understanding of the biological aspects of female sexual function, further research is needed in the physiology and pharmacology of peripheral (clitoral and vaginal) genital arousal in the animal model.

Objectives: To investigate the direct effect of ephedrine and cocaine on neurogenic contraction of penile trabecular smooth muscle. We also provide three case reports of patients who developed priapism secondary to using either cocaine or nonprescription weight loss formulations containing ephedrine. The use/abuse of cocaine has been associated with priapism. In addition, anecdotal evidence suggests that priapism may result from ephedrine use. However, the effects of cocaine and ephedrine on adrenergic regulation of cavernosal tissue and the potential role of sympathetic dysregulation in the development of priapism have not been studied., Methods: Isolated rabbit penile cavernosal tissue strips in organ bath preparations were subjected to electrical field stimulation (EFS) at varying frequencies (5 to 40 Hz) in the absence or presence of ephedrine (60 microg/mL) or cocaine (10 microM). Tissues were then subjected to EFS every 30 minutes for up to 20 hours., Results: Ephedrine and cocaine initially caused contractions in cavernosal tissue strips that persisted for several hours. EFS-induced contractions became attenuated over time in tissues treated with ephedrine or cocaine. Eventually, the contractile responses to EFS were not distinguishable from the basal tone, although the tissues remained responsive to exogenous phenylephrine., Conclusions: Functional activation of alpha-adrenergic receptors on trabecular smooth muscle does not appear to be impaired with prolonged cocaine or ephedrine exposure. However, chronic use of cocaine or ephedrine may deplete norepinephrine from sympathetic nerve terminals, leading to priapism.

The goal of this study was to investigate the effects of medical castration (luteinizing hormone-receptor hormone [LH-RH] agonist treatment) or surgical castration on erectile function in an animal model. New Zealand White male rabbits were either kept intact (control); surgically orchiectomized; or treated for 2, 4, or 8 weeks with the LH-RH agonist leuprolide acetate (107 microg/kg/mo). At 2 weeks, plasma testosterone levels of orchiectomized and leuprolide acetate-treated animals were 12.8% and 57.4% of intact control animals, respectively. Erectile function was assessed by continuously recording systemic arterial pressure (SAP) and intracavernosal blood pressure (ICP) and determining the ICP:SAP ratios in response to electrical stimulation of the pelvic nerve at varying frequencies (2.5-32 Hz). Androgen deprivation by surgical (orchiectomy) or medical (leuprolide acetate) castration reduced ICP at all frequencies tested but did not alter SAP. Administration of the phosphodiesterase type 5 inhibitor vardenafil (10 microg/kg) did not enhance ICP in surgically orchiectomized or leuprolide acetate-treated animals. Nitric oxide synthase and arginase activities in the corpus cavernosum were not significantly altered by surgical or medical castration. Further, Masson trichrome staining of erectile tissue from androgen-ablated animals showed a reduction in smooth muscle content. These data demonstrate that androgen deprivation achieved by surgical or medical castration adversely affects penile hemodynamics and erectile function without producing significant changes in the activities of nitric oxide synthase or arginase. We conclude that androgen deprivation produces structural alterations in the corpus cavernosum leading to corporal veno-occlusive dysfunction.

Objective: To determine the expression of P2Y(2) receptors in vaginal and cervical tissues and the effects of P2Y(2) receptor agonists INS45973 and INS365 on vaginal moisture., Design: Pilot in vivo and histological study using animal subjects., Setting: Experimental laboratory research., Animal(s): Female New Zealand White rabbits were used for in vivo studies and female cynomolgus monkey (Macaca fascicularis) was used for in situ hybridization., Intervention(s): Rabbits were kept intact or ovariectomized. Two weeks after ovariectomy, animals received daily vaginal instillation of vehicle or drugs for 16 days., Main Outcome Measure(s): Vaginal moisture was assessed in rabbits on 4 separate days during the treatment period. The P2Y(2) receptor mRNA distribution was assessed by in situ hybridization of monkey vagina and cervix., Result(s): Compared to control, vaginal moisture was significantly diminished in ovariectomized animals treated with vehicle. INS365 (8.1%) and INS45973 (0.9%) increased vaginal moisture in ovariectomized animals to levels that were comparable to or significantly higher than control animals, respectively. In situ hybridization studies indicated that P2Y(2) receptor mRNA was localized to endocervical and cervical gland, epithelium, and stratified squamous epithelium of the vagina., Conclusion(s): INS45973 and INS365 may interact with P2Y(2) receptors in the cervix and vagina to stimulate vaginal moisture in the estrogen (E)-deprived state. The P2Y(2) receptor agonists provide a potential nonhormonal alternative for treating vaginal dryness in postmenopausal women.

The EROS therapy device is FDA-approved for the treatment of women with sexual dysfunction and has been shown to improve sexual function and satisfaction. The aim of this study was to obtain objective information regarding the ability of the EROS Therapy device to induce clitoral and corpus spongiosum volumetric and hemodynamic changes following therapeutic use in women with sexual arousal disorder. Seven patients with sexual arousal disorder formed the study population. All seven subjects met inclusion and exclusion criteria, including having normal hormonal values at the time of the study. All seven subjects were able to comfortably operate the device. All seven reported either slight-to-moderate pleasure or orgasm at home with the device. We observed no adverse events. This study shows that EROS therapy is associated with significant increases in clitoral and corpus spongiosum diameter as well as with clitoral and corpus spongiosum peak systolic and end-diastolic velocity values.

The goal of this study was to investigate the effects of ovariectomy and estrogen replacement on vaginal tissue integrity and vaginal lubrication in basal conditions and in response to pelvic nerve stimulation (PNS). Two weeks after ovariectomy, female New Zealand White rabbits were administered vehicle or estradiol (200 micrograms/day) for an additional 2 weeks. Ovariectomy caused significant vaginal atrophy and diminished vaginal lubrication in the basal state and after PNS, compared to intact controls. Estrogen replacement normalized lubrication values and tissue wet weight to control levels. In conclusion, vaginal tissue integrity and lubrication are diminished by ovariectomy and are normalized by estrogen replacement.

Objective: Our purpose was to investigate the effects of ovariectomy and estradiol and testosterone treatment on sildenafil- induced changes in genital hemodynamics and vaginal lubrication., Study Design: Female New Zealand White rabbits were either kept intact or underwent ovariectomy. Two weeks after ovariectomy, animals were treated with vehicle, testosterone, or a combination of estradiol and testosterone for 14 days. Genital hemodynamics and vaginal lubrication were recorded at the end of the treatment period., Results: Ovariectomy caused a marked decrease in vaginal lubrication but did not significantly alter genital hemodynamics. In contrast to testosterone treatment of ovariectomized animals, estradiol treatment significantly increased genital blood flow and vaginal lubrication above that observed in control animals. Sildenafil administration caused a significant increase in genital hemodynamics irrespective of the hormonal status., Conclusion: This study suggests that estradiol but not testosterone modulates genital hemodynamics and that sildenafil enhances genital blood flow irrespective of hormonal status.

Limited studies are available concerning physiological and biochemical mechanisms involved in female sexual function and dysfunction. The paucity of physiological and biochemical data pertaining to genital sexual arousal function is attributed, in part, to lack of reliable experimental models and tools for the investigation of female sexual arousal. This review summarizes research efforts from a number of laboratories in which several experimental models have been established. These include the development of in vivo animal models, organ bath studies, and the establishment of cell cultures. The availability of such experimental model systems have facilitated efforts aimed at defining the neurotransmitters responsible for vaginal smooth muscle relaxation, the role of sex steroid hormones and their receptors in modulating genital hemodynamics, smooth muscle contractility, and neurotransmitter receptor expression. A comprehensive and integral understanding of female sexual function requires detailed investigation of the vascular, neurological (central and peripheral), and structural components of this complex physiological process.

Although the psychosocial and relationship aspects of female sexuality have been extensively investigated, studies concerning the anatomy, physiology and pathophysiology of female sexual function and dysfunction are limited. The paucity of biologic data may be attributed to a lack of reliable experimental models and tools for investigating female sexual function and to limited funding, which is critical for developing experimental approaches. Research efforts by several investigators in different laboratories have been establishing experimental models needed for investigating the physiologic mechanisms involved in the genital arousal response of sexual function. These experimental models have permitted assessment of genital hemodynamics, vaginal lubrication, regulation of genital smooth muscle contractility and signaling pathways, providing preliminary information about the role of neurotransmitters and sex steroid hormones in sexual function. Further research is needed to define the neurotransmitters responsible for vaginal smooth muscle relaxation and the role of sex steroid hormones and their receptors in modulating genital hemodynamics, smooth muscle contractility, and neurotransmitter receptor expression. Finally, a global and integral understanding of the biologic aspects of female sexual function requires investigation of the vascular, neurologic (central and peripheral), and structural components of this extremely complex physiologic process.

Vardenafil and sildenafil are potent and specific phosphodiesterase type 5 (PDE 5) inhibitors. In human penile cavernosal smooth muscle cells, we have previously shown that vardenafil has a lower biochemical inhibition constant (Ki) than sildenafil. In this study, we compared the efficacy of vardenafil and sildenafil in facilitating penile erection in a rabbit model. Penile erections were elicited by submaximal (2.5 or 6 Hz) pelvic nerve stimulation (PNS) repeated every 5 minutes for 30 minutes with or without intravenous (i.v.) administration of vardenafil (1-30 microg/kg) or sildenafil (10-30 microg/kg). Erectile response was assessed by continuously recording intracavernosal pressure (ICP) and systemic arterial pressure (SAP). All data were expressed as a ratio of ICP:SAP. I.v. administration of either PDE 5 inhibitor facilitated PNS-induced erection and increased ICP:SAP in a dose-dependent manner, reaching peak response at approximately 5 minutes. However, the threshold dose at which facilitation of erection occurred was lower for vardenafil (3 microg/kg) than for sildenafil (10 microg/kg). At the 10-microg/kg dose (i.v.), the response duration was significantly greater with vardenafil (169 +/- 23 seconds) than with sildenafil (137 +/- 31 seconds). Direct intracavernosal (i.c.) injection of 1-30 microg/kg vardenafil or sildenafil also caused dose-dependent increases in ICP:SAP in the absence of PNS. Response durations increased in a dose-dependent manner and lasted more than 5 times that of i.v. drug administration coupled with PNS. Irrespective of the route of administration (i.c. or i.v.), at equivalent doses, vardenafil was significantly more efficacious than sildenafil in facilitating pelvic nerve-mediated penile erection and in eliciting erection in the absence of PNS. The increases in ICPs occurred more quickly, were of larger magnitude, and were sustained for longer durations for vardenafil than for sildenafil. On the basis of the biochemical data and physiological responses from this study, further clinical evaluation of vardenafil as treatment for erectile dysfunction is warranted.

Objective: In women, androgens modulate the physiological function of many reproductive and sexual organs, including the ovaries, uterus, vagina, oviducts, clitoris, and mammary gland. In this article, we review the mechanisms of androgen action and discuss new data on the effects of androgens in vaginal and clitoral tissues., Main Outcome Measure(s): In this study, we characterized the androgen receptor expression in rabbit vaginal tissues from control and ovariectomized animals treated with or without androgen replacement therapy. We investigated the effects of androgen deprivation and replacement on the expression and activity of nitric oxide synthase and arginase and on vaginal smooth muscle contractility., Result(s): Androgens enhanced nitric oxide synthase activity and down-regulated arginase activity in proximal vagina. Estrogens down-regulated nitric oxide synthase activity and increased arginase activity in distal vagina. Androgens facilitated vaginal smooth muscle relaxation to electric field stimulation and vasoactive intestinal polypeptide, whereas estrogens attenuated vaginal tissue relaxation to electric field stimulation and to vasoactive intestinal polypeptide., Conclusion(s): These observations suggest that androgens may play an important role in modulating the physiology of vaginal tissue and contribute to female genital sexual arousal.

This study was designed to determine the utility and validity of laser oximetry in measuring changes in penile hemodynamics. Anesthetized male New Zealand White Rabbits were divided into 2 groups, and penile hemodynamics were assessed by either laser oximetry (oxyhemoglobin, deoxyhemoglobin concentration, and oxygen saturation) or intracavernosal pressure (ICP) monitoring during penile erection induced by pelvic nerve stimulation (PNS) or intracavernosal administration of phentolamine, nitroprusside, papaverine, or sildenafil. PNS caused significant frequency-dependent increases in penile ICP. PNS also caused significant increases in penile tissue oxyhemoglobin concentrations and tissue oxygen saturation in a frequency-dependent manner. The changes in oxyhemoglobin concentrations and oxygen saturation correlated with frequency-dependent increases in ICP. Intracavernosal vasoactive drug administration produced significant increases in ICP, tissue oxyhemoglobin concentration, oxygen saturation, and duration of response as a function of increasing drug concentration. Laser oximetry permits reproducible and valid assessment of changes in penile hemodynamics comparable to conventional ICP measurements. Thus, we consider laser oximetry a reliable technique in evaluating penile hemodynamics. Its sensitivity in detecting small changes in oxyhemoglobin concentration and its noninvasive nature make it advantageous over invasive methods such as ICP monitoring and laser Doppler flowmetry.

Female sexual dysfunction is a highly prevalent, multicausal, and multidimensional medical problem that has a major impact on quality of life and interpersonal relationships. It is hypothesized that genital arousal disorder is caused by diminished arterial blood flow within the hypogastric arterial bed. This hypothesis may explain the pathophysiologic mechanisms in older patients with vascular risk factors, but it does not account for either the prevalence or the mechanisms of arousal disorders seen in young women with no vascular risk factors. Hormonal imbalances may be important contributing factors to the pathophysiologic mechanisms involved in female arousal disorders. Androgens modulate the growth and function of female genital sexual organs included the labia, vagina, and clitoris. This article discusses the potential role for androgens in facilitating female genital sexual arousal.

Perineal trauma can occur in both genders, however, data supporting the relationship between sexual dysfunction and blunt perineal trauma in women is lacking. This study reviewed the patient characteristics of women with sexual dysfunction who also had a history of blunt perineal trauma. A neurogenic form of sexual dysfunction has been implicated, with primary complaints of orgasm disorder and abnormalities noted on genital sensory testing. Further research in this area is needed.

During our evaluations of women with sexual dysfunction, we have seen many with low interest, arousal, and orgasmic capabilities with associated personal distress and diminished genital sensation and blood flow following sexual stimulation. Laboratory evaluation of these women has revealed normal estrogen but androgen values that were either below or in the lower quartile of the physiologic range. Androgen insufficiency and sexual dysfunction have been the working diagnoses in these women. Although many treatment options currently are available for this syndrome, there are limited data concerning safety and efficacy. The aim of this retrospective, Institutional Review Board (IRB)--approved, single-institution study was to report on the androgen and questionnaire results from a series of patients who underwent androgen replacement therapy with dehydroepiandrosterone for treatment of androgen insufficiency and sexual dysfunction. This study revealed that there was a significant decrease in sexual distress, a significant increase in sexual function in the domains of desire, arousal, lubrication, satisfaction, and orgasm, and a normalization to values within the physiologic range in the following androgens measured: total testosterone, free or bioavAilable testosterone, DHEA, DHEA-S, and androstenedione. Side effects included increased facial hair (11%), weight gain (7%), acne (5%), temporary breast tenderness (1%), loss of head hair (1%) and skin rash (1%). Preliminary results suggest that androgen replacement therapy with dehydroepiandrosterone is a safe and effective treatment for androgen insufficiency and female sexual dysfunction. However, further research is needed, including prospective, multi-institution, placebo-controlled double-blind studies.

There have been limited literature reports concerning the epidemiological characteristics of female patients who present for initial evaluation of sexual health problems to an outpatient sexual health clinic. This study is a single-institution, retrospective, IRB-approved, observational assessment of 250 female patients undergoing management for sexual dysfunction. In our clinic, women with sexual dysfunction were, in general, young, healthy, and free of vascular risk factors; complained of an acquired multidimensional combination of decreased desire, arousal, and orgasm; and had significantly low serum androgen levels. More research in the management of women with sexual health problems is needed.

Physical examination of the genitalia was performed during an evaluation of women with sexual health problems. Cephalad displacement of the right and left labia minora enables full retraction of the clitoral prepuce and complete exposure of the glans clitoris, under normal circumstances. We defined clitoral examination as abnormal when the cephalad force resulted in varying degrees of incomplete foreskin retraction and limited exposure of the glans clitoris. The pathophysiology is likely to be secondary to recurrent vulvar dermal infections of blunt trauma changing prepucial elasticity. Clitoral phimosis, a previously undiagnosed physical finding, was identified in 22% of the women. Other than its link to sexual pain, the clinical significance of this finding, in particular the relation to diminished sensitivity and impaired orgasmic capability, is unclear at this time.

There have been limited anatomic and physiological investigations of the female sexual arousal response. A broader understanding of the physiologic mechanisms of female sexual arousal function is required to improve the management of women with sexual dysfunction. Three experimental test systems have been developed to understand better the biochemical and physiological mechanisms of female sexual arousal response. An in vivo animal model was developed to record physiological and hemodynamic changes in the clitoris and vagina following pelvic nerve stimulation and administration of vasoactive agents and physiological modulators. In vitro organ baths of clitoral and vaginal tissue were utilized to investigate mechanisms involved in the regulation of smooth muscle contractility. In addition, primary cell cultures of human and animal clitoral and vaginal smooth muscle cells were developed to investigate signal transduction pathways modulating smooth muscle tone. In vivo studies revealed hemodynamic changes in vagina and clitoris in response to pelvic nerve stimulation, vasodilators and physiological modulators. Organ bath studies have demonstrated that clitoral and vaginal smooth muscle tone is affected by non-adrenergic and non-cholinergic neurotransmitters, and the presence of functional alpha 1 and alpha 2 adrenergic receptors in these tissues has been established through biochemical studies. These changes are regulated by the tone of vascular and non-vascular smooth muscle in the vagina and clitoris. Primary cell culture studies have suggested that several physiological modulators such as vasoactive intestinal polypeptide (VIP), nitric oxide (NO), and prostaglandin E (PGE) regulate vaginal smooth muscle contractility. Data from experimental models have provided a preliminary understanding of the mechanisms of the female sexual arousal response.

Purpose: Use of a nonmedical, catalogue type vacuum erection device resulted in a case of vacuum induced vasculogenic impotence and Peyronie's disease., Materials and Methods: A 66-year-old potent man used a nonmedical vacuum erection device (cylinder plus a hand pump without a pressure-release valve and a doughnut-shaped ring at the base without tension bands) after having achieved a spontaneous rigid erection. The resultant excessive overinflation of the penis was followed by dorsal curvature, diminished rigidity and decreased erectile maintenance., Results: Physical examination revealed a dorsal mid shaft Peyronie's plaque. Nocturnal penile tumescence testing and office injection testing were abnormal and demonstrated partial, short-lived, dorsally curved erections. Dynamic pharmaco-cavernosometry and pharmaco-cavernosography established vasculogenic impotence with site-specific crural (unrelated to the Peyronie's plaque) veno-occlusive dysfunction and dorsal penile curvature., Conclusions: Vacuum erection devices create pulling forces on the penis. We estimate that the pulling forces in this case were prohibitively high (approximately 29 pounds) due to absence of a pressure-release valve and to the preexistent erection at vacuum application. These intense pulling forces are hypothesized to have damaged the tunica in the mid shaft (Peyronie's disease) and the crus (veno-occlusive dysfunction), the latter being the site of attachment of the corpora to the ischiopubic ramus and a most likely location for high magnitude pulling forces to exert an abnormal injury effect. The patient underwent a Nesbit plication procedure and presently performs self-injection for satisfactory sexual activity.

1. This study was designed to determine the role of sodium-potassium adenosine triphosphatase (Na(+)-K(+)-ATPase) in the regulation of human corpus cavernosum smooth muscle contractility by nitric oxide (NO). In addition, we determined if the modulation of Na(+)-K(+)-ATPase activity by NO is dependent on the increase in intracellular cyclic GMP concentration. 2. The effect of NO donors, sodium-nitroprusside (SNP) and S-nitroso-glutathione (S-NO-Glu), and a permeable cyclic GMP analogue, 8-bromo-cyclic GMP, on Na(+)-K(+)-ATPase activity (measured as ouabain-sensitive 86Rb-uptake) was studied in human cultured corpus cavernosum smooth muscle cells (HCCSMC). In addition, the effect of the cyclic GMP lowering agent, methylene blue, on NO-induced increase in Na(+)-K(+)-ATPase activity was studied. 3. SNP (1 microM) caused time-dependent increases in ouabain-sensitive Rb-uptake (33-72%) over 2-20 min in HCCSMC. The stimulation of ouabain-sensitive Rb-uptake by SNP was concentration-dependent (30 and 102% with 0.1 and 1 microM SNP, respectively). Similarly, significant increases in ouabain-sensitive Rb-uptake were obtained with 1 and 10 microM S-NO-Glu. In contrast, incubation of HCCSMC with 8-bromo-cyclic GMP (100 microM) did not increase ouabain-sensitive Rb-uptake. 4. S-NO-Glu induced-increase in intracellular cyclic GMP synthesis, but not the increase in ouabain-sensitive Rb-uptake, was completely inhibited by methylene blue in HCCSMC. 5. The Na(+)-K(+)-ATPase inhibitor, ouabain, caused a concentration-dependent increase in tension (0.5 to 2 fold) in tissues contracted with 15 mM KCl. SNP and S-NO-Glu caused a concentration-dependent relaxation (concentration required to cause half maximal relaxation (ED50) = 0.04 and 0.2 microM, respectively) of HCC strips contracted with 15 mM K+. Ouabain (0.1 to 10 microM) inhibited the response to SNP and S-NO-Glu by shifting the concentration-response curves to the right and preventing full smooth muscle relaxation.6. These results indicate that the activity of Na+-K+-ATPase modulates the contractility of HCC smooth muscle, and that NO stimulates Na+-K+-ATPase activity in HCCSMC independently of its ability to increase the intracellular cyclic GMP concentration. They also suggest that stimulation of Na+-K+-ATPase activity plays an important role in NO-induced relaxation of HCC smooth muscle

A 9 1/2-year pharmaco-cavernosometry/pharmaco-cavernosography and pharmaco-arteriography study was performed in 131 men with persistent changes in erectile function following blunt pelvic or perineal trauma. The goal was to determine the incidence of hemodynamic impairment, and to characterize the location and pattern of abnormal venous drainage. Corporeal veno-occlusive dysfunction was identified in 62% of the cases and cavernous artery insufficiency in 70%. Pharmaco-cavernosography revealed abnormal venous drainage confined to the proximal corpora in 91% of the cases. Patients with pelvic trauma had significantly more abnormal sites of venous drainage (3 or more sites in 61%) and more severe degrees to which venous structures filled with contrast medium (23% had 3+ degree of luminal filling) than did patients with perineal trauma (61% had 1 or 2 sites of venous drainage and 92% had 1+ or 2+ degree of luminal filling). Pharmaco-arteriography revealed site specific arterial occlusive lesions consistent with the site of impact. Traumatic vasculogenic impotence is hypothesized as being the result of direct impact injury to the fixed proximal corpora and its arterial inflow bed. The exerted perineal impact force is estimated to range from 50 to 500 pounds, depending on the weight of the individual, height of the fall, speed at contact and surface hardness. Traumatic veno-occlusive dysfunction is theorized to be the consequence of focal intracavernous wound repair and permanent focal alterations in erectile tissue compliance. Traumatic vasculogenic impotence afflicts an estimated 600,000 American men of whom 250,000 have sports-related injuries. Future consideration should be given to the development of appropriate protective perineal equipment.