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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.

The effects of subphysiological and physiological levels of estradiol on vaginal blood flow and estrogen receptor were investigated.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.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.Estradiol is crucial for maintaining optimal vaginal blood flow in the rat. Lower levels of plasma estradiol trigger compensatory ERalpha up-regulation.

Effective medical management of female genital sexual arousal disorder necessitates understanding of biochemical and physiological mechanisms regulating female sexual arousal responses via central and peripheral pathways. The complexity of the female sexual response and the limited experimental models available has severely hampered progress in this field. Recent studies have begun to unravel peripheral biochemical mediators involved in regulating genital engorgement/swelling and lubrication. Research in this area should identify molecular targets for pharmacotherapy of female sexual arousal dysfunction.

Sexual dysfunction (SD) in women is a multifactorial condition with anatomical, physiological, medical, psychological and social components. Well-designed, random-sample, community-based epidemiological investigations of women with SD are limited. Current data reveal that up to 76% of women have some type of SD [1,2]. Population census data from the USA suggest that approximate to 10 million American women aged 50-74 years self-report complaints of diminished vaginal lubrication, pain and discomfort during intercourse, decreased arousal, and difficulty achieving orgasm. Laumann et al. [3] found that SD is more prevalent in women (43%) than in men (31%), and is associated with various psycho-demographic characteristics, e. g. age, education, and poor physical and emotional health. More importantly, women's SD (WSD) is associated with negative experiences in sexual relationships. Recently, Brock et al. [4] reported the results of an international survey aimed at assessing both the prevalence and predictors of SD among mature men and women. Among a population of 4507 subjects, decreased sexual interest was reported by 34% of women and 18% of men; moreover, 19% of women and 11% of men reported that they did not consider sex pleasurable. Of the women interviewed, 23% reported inadequate lubrication, with a significant increase in this complaint in women aged 50-69 years [4].

Androgen insufficiency is a recognized cause of sexual dysfunction in men and women. Age-related decrements in adrenal and gonadal androgen levels also occur naturally in both sexes. At present, it is unclear if a woman's low serum androgen level is a reflection of the expected normal age-related decline or indicative of an underlying androgen-deficient state. We studied premenopausal women with no complaints of sexual dysfunction to help define a normal female androgen profile. In all, 60 healthy, normally menstruating women, ages 20-49 y, were studied. The Abbreviated Sexual Function Questionnaire was administered along with a detailed interview. Radioimmunoassay measurements of morning serum testosterone (T), free testosterone (fT), dehydroepiandrosterone-sulfate (DHEAS), sex hormone-binding globulin (SHBG), and free androgen index (FAI) were measured during days 8-15 of the menstrual cycle. In women 20-49 y old without complaints of sexual dysfunction, serum androgen levels exhibit a progressive stepwise decline. Comparing values obtained in women age 20-29 y to those obtained in women 40-49 y, specific hormone decrements were DHEAS 195.6-140.4 microg/dl, serum T 51.5-33.7 ng/dl, fT 1.51-1.03 pg/ml. SHBG did not change significantly in women in this age group. The FAI reflected the age-related decrease in female androgen levels. The framework for the development of a female androgen profile in women with no complaints of sexual dysfunction has been established, and an age-related decrease in testosterone and its adrenal precursor, DHEAS, has been demonstrated. The FAI mirrors these decreases and its usefulness in clinical practice is confirmed. A precipitous decline in all androgens occurs after the decade of the 20s, yet SHBG does not show a significant change throughout the premenopausal years.

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.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.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, p0.00001) 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, p0.00001).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.

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 μg/mL) or cocaine (10 μM). 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.

As many as 10 million American women 50 to 74 years of age describe reduced vaginal lubrication, uncomfortable or frankly painful intercourse, decreased arousal, and difficulty reaching orgasm. These symptoms have been associated with the postmenopausal drop in estrogen levels. The P2Y 2 receptor agonists are purinergic receptor ligands currently under study for their prosecretory effects in numerous clinical settings. Stimulation of P2Y 2 receptors activates phospholipase C, prompting intracellular release of calcium that increases surface liquid and hydrates secretions. This study examined the potential role for P2Y 2 receptor agonists in treating vaginal dryness. Two weeks after ovariectomy, rabbits received daily instillations of one of two agonists, 0.9% INS45973 or 8.1% INS365, for 16 days, while control animals received vehicle only. Swabs were used as moisture probes. In situ hybridization studies were carried out to estimate receptor mRNA in vaginal and cervical tissues from female cynomolgus monkeys. Vaginal moisture was significantly reduced after ovariectomy in vehicle-exposed rabbits. Both P2Y 2 receptor agonists increased moisture in ovariectomized animals. Moisture levels were comparable to those in control animals when INS365 was administered and significantly higher than in controls with INS45973. Ovariectomy resulted in minimal inflammation, which was not observed when animals were given either agonist. The cytoplasm of cells in both cervical gland and endocervical epithelium, but not the stroma, exhibited positive staining for receptor mRNA. Examination of vaginal tissue samples showed positive staining in the cytoplasm of stratified squamous epithelial cells, but not in the submucosa or muscularis. Synthetic P2Y 2 receptor agonists are able to increase vaginal moisture in estrogen-deprived animals, and they could relieve postmenopausal vaginal dryness by increasing mucin production as well as augmenting pelvic blood flow. This approach might be safer than systemic or topical estrogen replacement in high-risk women.

There are limited hemodynamic data in women with arousal or orgasmic disorders and even fewer normative control hemodynamic data in women without sexual dysfunction. In addition, there is limited experience with topical vasoactive agents (used to maximize genital smooth muscle relaxation) applied to the external genitalia during hemodynamic evaluations. The aim of this study was to report duplex Doppler ultrasound clitoral cavernosal arterial changes before and after topical PGE-1 (Alprostadil) administration in control women and in patients with arousal and orgasmic sexual disorders. We found that women with sexual arousal and orgasmic disorders had significantly (p

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.

There are limited hemodynamic data in women with arousal or orgasmic disorders and even fewer normative control hemodynamic data in women without sexual dysfunction. In addition, there is limited experience with topical vasoactive agents (used to maximize genital smooth muscle relaxation) applied to the external genitalia during hemodynamic evaluations. The aim of this study was to report duplex Doppler ultrasound clitoral cavernosal arterial changes before and after topical PGE-1 (Alprostadil) administration in control women and in patients with arousal and orgasmic sexual disorders. We found that women with sexual arousal and orgasmic disorders had significantly (p < 0.05) diminished clitoral peak systolic and end diastolic velocity responses compared to controls. Further research is needed to establish the diagnostic role of topical vasoactive agents in the hemodynamic evaluation of women with sexual dysfunction.

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.

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 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.

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.

We present a case of corpus cavernosum hematoma mimicking priapism. A 42-year-old man presented to the emergency room with penile pain and partial erection. Examination revealed partial erection and palpable space-occupying lesion of the corpus cavernosum without lymphadenopathy. Malignant workup was negative. Imaging assisted in diagnosis of unilateral hematoma of the corpus cavernosum. The lesion spontaneously resolved without the need for intervention.

Introduction Penile revascularization is a surgical treatment option for erectile dysfunction (ED) in healthy individuals due to a focal arterial occlusion in the absence of generalized vascular disease. Most described failures have been attributed to graft stenosis or disruption of the anastomosis. Aim We report a novel phenomenon called Penile Artery Shunt Syndrome that contributed to persistent ED in a patient after penile microvascular arterial bypass surgery. Methods A 26‐year‐old man presented for evaluation of long‐standing ED, which was attributed to trauma sustained 12 years earlier. He had difficulty obtaining and maintaining erections despite oral pharmacotherapy. Clinical data related to the case were studied, analyzed, and reviewed with urologic and radiologic specialists at multiple centers that collaborated in the care of this patient. Main Outcome Measures Penile duplex ultrasound peak systolic velocities and five‐item International Index for Erectile Function questionnaire scores were the main outcome measures. Results Initial diagnostic workup of the patient confirmed severe insufficiency of the left cavernosal artery, with no evidence of venous leak. The patient underwent penile microvascular arterial bypass surgery with anastomosis of the left inferior epigastric artery to the left dorsal penile artery. The patient had persistence of severe ED despite patent anastomosis by penile duplex ultrasound. Subsequent arteriography revealed an arterial shunt due to an aberrant obturator artery arising from the donor inferior epigastric artery. The patient underwent embolization of the aberrant obturator artery, with resolution of the shunt and marked improvement in erectile function. Conclusions The presence of an aberrant obturator artery arising from the inferior epigastric artery may predispose to persistent ED after revascularization due to the creation of a shunt phenomenon. Pelvic arteriography may be useful in identifying anomalous anatomic considerations prior to penile revascularization and to evaluate patients with persistent postoperative ED. Pavlinec JG, Hakky TS, Yang C, Massis K, Munarriz R, and Carrion RE. Penile Artery Shunt Syndrome: A novel cause of erectile dysfunction after penile revascularization surgery. J Sex Med 2014;11:2338‐2341.

The goal of this study was to assess the utility of existing and new techniques for characterizing and measuring hemodynamic changes in the vagina and clitoris in response to pelvic nerve stimulation (PNS) in an animal model. Using female New Zealand White rabbits, we measured the following parameters before, during, and after PNS at 4, 16, and 32 hertz (Hz): clitoral hemoglobin (Hb) content by laser oximetry, clitoral blood flow by laser Doppler flowmetry, vaginal luminal pressure of upper and lower segments, and clitoral intracavernosal pressure. Clitoral tissue concentrations of total and oxygenated hemoglobin (oxy-Hb) increased in a frequency-dependent manner while deoxygenated hemoglobin (deoxy-Hb) concentration decreased. The duration of the responses at 16 and 32 Hz were significantly greater than at 4 Hz. Clitoral blood flow increased significantly only at 32 Hz with a prolonged response duration, relative to 4 Hz. PNS caused vaginal luminal pressure changes that were highly variable, but qualitatively different, between the upper and lower regions. Clitoral intracavernosal pressure did not change significantly in response to PNS. Measurement of changes in tissue Hb content by the novel technique of laser oximetry provides a direct assessment of blood flow in a noninvasive manner and may prove to be a powerful tool in evaluating hemodynamic aspects of the female genital sexual response.

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.

Bicycle riding is a popular and environmentally friendly mode of transportation and exercise with obvious health benefits that include cardiovascular health, weight loss, relaxation, and improved quality of life. However, bicycle riding is also associated with health risks, including erectile dysfunction. The overall aim of this literature review is to summarize the accumulating medical data concerning the association between bicycle riding and erectile dysfunction.

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 percent of the cases and cavernous artery insufficiency in 70 percent.Pharmaco-cavernosography revealed abnormal venous drainage confined to the proximal corpora in 91 percent of the cases. Patients with pelvic trauma had significantly more abnormal sites of venous drainage (3 or more sites in 61 percent) and more severe degrees to which venous structures filled with contrast medium (23 percent had 3+ degree of luminal filling) than did patients with perineal trauma (61 percent had 1 or 2 sites of venous drainage and 92 percent had 1+ or 2+ degree of luminal filling). Pharmaco-arteriography reveale...

Blunt pelvic and perineal trauma has been previously reported to result in site-specific veno-occlusive dysfunction and/or site-specific cavernosal artery insufficiency. We herein describe a case of erectile dysfunction in a young previously potent amputee. We postulate that the erectile dysfunction is associated with a newly described form of blunt trauma, that is, site-specific compression from a perineal weight-bearing lower extremity above-knee prosthetic device. It is hypothesized that when the force exerted by the above-knee prosthesis is directed medially towards the ischiopubic ramus, the penile crura and common penile arterial blood supply become susceptible to crush-like injury, since they are in fixed anatomic locations in the perineum sandwiched between the compressive force and the bone. Clinical evaluation of the erectile dysfunction in this patient revealed site-specific corporal veno-occlusive dysfunction and site-specific common penile arterial occlusive pathology in the precise region of the contact of the above-knee prosthesis with the perineum. Further research is needed in above-knee prosthesis design to prevent erectile dysfunction.

Introduction Robotically assisted laparoscopic radical prostatectomy (RALP) provides decreased surgical morbidity and faster recovery for patients, but has not significantly changed the incidence of erectile dysfunction and many post RALP patients may require penile prosthesis surgery. Aim To make physicians aware of the anatomical changes after RALP in comparison to traditional retropubic radical prostatectomy and to make suggestions for safer reservoir placement. Main Outcome Measures Reservoir location after RALP. Methods A 68 year-old patient with severe vasculogenic ED refractory to pharmacologic management following RALP underwent a 3-piece penile prosthesis insertion surgery and laparoscopic right lower abdominal hernia repair. Laparoscopy revealed an intraperitoneal reservoir that was overlying the sigmoid colon with multiple diverticula. The reservoir was laparoscopically repositioned in the dependent pelvis away from the diverticula and the pelvic vessels. Results The patient's postoperative course was uneventful without any postoperative complications (2 year follow up). Conclusions The altered anatomy of the space of Retzius following RALP will likely result in significantly more cases of inadvertent intraperitoneal reservoir placement. Surgeons performing inflatable penile prosthesis surgery should be aware of these anatomical changes and prepared to consider ectopic reservoir placement when necessary. Sadeghi-Nejad H, Munarriz R, and Shah N. Intra-abdominal reservoir placement during penile prosthesis surgery in post-robotically assisted laparoscopic radical prostatectomy patients: A case report and practical considerations. J Sex Med 2011;8:1547–1550.

Penile microarterial bypass surgery (MABS) may be the only treatment capable of restoring normal erectile function without 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 has resulted in this surgery being considered experimental. In addition, poor reimbursements, long surgical time, and the need for microsurgical expertise have lead to infrequent penile revascularization procedures. Using the criteria for the Arterial Occlusive Disease Index patient, only 4 of 31 manuscripts met the criteria. 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% to 91%. We recently published the largest long-term outcome MABS study using validated instruments. We documented MABS provides long-term improvements in erectile function, depression, and overall satisfaction in well-selected patients. The Members of the Erectile Dysfunction Guideline Update Panel consider: “Arterial reconstructive surgery is a treatment option only in healthy individuals with recently acquired erectile dysfunction secondary to a focal arterial occlusion and in the absence of any evidence of generalized vascular disease.”

Introduction: The role of androgens in sexual function and in particular in erectile physiology remains controversial. The aim of this chapter is to review the preclinical and clinical data on the impact of androgen deprivation in male sexual functioning since androgen ablation is the main treatment option for men with advanced prostate cancer and a critical component of radiation therapy for localized prostate cancer.

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.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).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.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.

Penile epithelioid hemangioma is a very rare benign vascular neoplasm of unclear etiology. To the best of our knowledge, only 28 cases in the literature have been reported to date. We report a case of epithelioid hemangioma of the penis in a 41-year-old man with a painful penile mass. The presented case exemplifies the importance of establishing a correct diagnosis through appropriate histologic analysis, as epithelioid hemangiomas are often misdiagnosed as two highly malignant tumors, epithelioid hemangioendothelioma and epithelioid angiosarcoma. Establishing benignancy is crucial in order to avoid inappropriate and overly aggressive treatment.

We report the case of a 49-year-old man presenting with a recurrent penile fracture 1-year after undergoing delayed repair for a previous penile fracture. To the authors' knowledge, this case represents the first documented instance of repeat fracture occurring after delayed repair. Risk factors for repeat penile fracture are not well documented due to the rarity of this condition. A review of literature regarding repeat penile fracture and the impact of delayed repair is discussed.

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 [ 3 H]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 [ 3 H]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 µg) was 100% effective with no adverse events or significant changes in vital signs. In addition, two patients with ischemic priapism for ≥36 hours were successfully treated with high‐dose intracavernosal phenylephrine (mean dose 45,000 µg) 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. Wen CC, Munarriz R, McAuley I, Goldstein I, Traish A, and Kim N. Management of ischemic priapism with high‐dose intracavernosal phenylephrine: from bench to bedside. J Sex Med 2006;3:918–922.

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.To retrospectively investigate SHBG levels before and after discontinuation of OC use.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 and120 (mean 196) days after discontinuation of OCs.A total of 124 premenopausal women with sexual health complaints for6 months met inclusion/exclusion criteria. Three groups of women were defined: (i) "Continued-Users" (N = 62; mean age 32 years) had been on OCs for6 months and continued taking them; (ii) "Discontinued-Users" (N = 39; mean age 33 years) had been on OCs for6 months and discontinued them; and (iii) "Never-Users" (N = 23; mean age 36 years) had never taken OCs.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; P0.0001). 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; P0.0001 for120 days).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.

Despite availability of outcome measures and scales for assessing erectile dysfunction (ED) treatment efficacy, guidelines are not available for assessing broader therapeutic outcomes or defining treatment failure in ED. An International Consensus Advisory Panel was convened to develop guidelines, definitions and a new algorithm for evaluating treatment effectiveness in ED. These new guidelines are recommended for use in both research and clinical practice. A multidisciplinary, international panel, consisting of 11 senior researchers and clinicians, was convened to address pertinent issues concerning therapeutic outcome assessment for ED. The panel utilized a modified Delphi method of consensus development and proposed a new model for outcomes assessment. This model is inherently testable, using existing instruments and current methods of assessment. Following a comprehensive literature review and discussion, the Panel recommended adoption of a new treatment effectiveness conceptual framework or theoretical model for assessing therapeutic outcomes in ED. Treatment effectiveness is presumed to be a combined function of two other factors, treatment response and treatment satisfaction. Treatment response is based on the combined assessment of efficacy and tolerability, and treatment satisfaction on the combined assessment of patient and partner satisfaction. Taken together, these two domains define an overall domain of treatment effectiveness. This therapeutic index would be derived by independently assessing treatment efficacy and satisfaction by means of event logs, questionnaires or the more typical patient interview methods. In conclusion, the Ad Hoc Advisory Consensus Panel recommends adoption of a new framework or conceptual model for conducting ED outcome trials or clinical research. The concept of 'treatment effectiveness' is proposed as a new 'umbrella concept' or distal outcome to be evaluated.

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.

Androgen insufficiency has been associated with decreased libido and arousal in postmenopausal women, but rarely has been evaluated in healthy premenopausal women. In all, 32 healthy premenopausal women were enrolled in this study, 18 with one or more complaints of sexual dysfunction and 14 without. Assays of ovarian and adrenal androgens were measured before and after ACTH stimulation. The women with complaints of sexual dysfunction had significantly lower adrenal androgens than did the control women. There were no differences in the basal ovarian androgens or cortisol levels. After ACTH, both groups stimulated cortisol as well as adrenal and ovarian androgens. In conclusion, premenopausal women with complaints of sexual dysfunction had lower adrenal androgen precursors and testosterone than age-matched control women without such complaints. Further study is required to determine how lower adrenal androgens contribute to female sexual dysfunction.

The role of steroid hormones in regulating vaginal smooth muscle contractility was investigated. Rabbits were kept intact or ovariectomized. After 2 weeks, animals were continuously infused with vehicle or supraphysiological levels of testosterone (100 microg/day), or estradiol (200 microg/day), for an additional 2 weeks. The distal vaginal tissue was used to assess contractility in organ baths and changes in tissue structure were assessed by histology. Ovariectomized animals infused with vehicle exhibited significant atrophy of the muscularis and decreased epithelial height, resulting in thinning of the vaginal wall. Estradiol infusion increased epithelial height, comparable to that of intact animals, but only partially restored the muscularis layer. In contrast, testosterone infusion completely restored the muscularis layer, but only partially restored the epithelial height. In vaginal tissue strips contracted with norepinephrine and treated with bretylium, electrical field stimulation (EFS) caused frequency-dependent relaxation that was slightly attenuated with vehicle, significantly inhibited with estradiol and significantly enhanced with testosterone. VIP-induced relaxation was slightly attenuated in tissues from vehicle and estradiol-infused groups, but was enhanced in tissues from testosterone-infused animals. Contraction elicited by EFS or exogenous norepinephrine was not significantly altered with ovariectomy or steroid hormone infusion when data were normalized to potassium contraction. However, the tissue from testosterone-infused animals developed significantly greater contractile force to norepinephrine. These observations suggest that steroid hormones may be important regulators of vaginal tissue structure and contractility.

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.

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.

Nitric oxide synthase (NOS) and arginase have been shown to regulate nitric oxide (NO) production reciprocally in genital tissues. In animal models, NO is an important regulator of vaginal blood flow and vaginal wall contractility. In this study, we investigated the modulation of NOS and arginase activities by estrogens and androgens in the proximal and distal rabbit vagina. In intact control animals, total NOS activity was higher in the proximal (528+/-78 pmol/mg protein) than the distal (391+/-44 pmol/mg protein) vagina. However, arginase activity was higher in the distal (206+/-8 nmol/mg protein) than the proximal (64+/-5 nmol/mg protein) vagina. Ovariectomy enhanced NOS activity in the proximal but not distal vagina with concomitant decrease in arginase activity in both the proximal and distal vagina. In ovariectomized rabbits, replacement with 5alpha-dihydrotestosterone (DHT) or Delta5-androstenediol (Adiol) increased NOS activity beyond that observed in ovariectomized rabbits receiving vehicle. In contrast, DHT and Adiol treatment reduced arginase activity more than that of the ovariectomized rabbits receiving vehicle. Testosterone exhibited inconsistent effects on NOS and arginase activity in the distal and proximal vagina. Estradiol replacement in ovariectomized animals reduced NOS activity in the proximal vagina down to levels that were comparable to intact control animals. However, estradiol positively modulated arginase activity in the distal vagina. Western blot analyses indicated that in the proximal vagina, neural NOS protein levels paralleled the changes observed in enzyme activity. These observations suggest that steroid hormones differentially regulate NOS and arginase activities of the proximal and distal regions of the vagina. Although estrogen treatment reduced total NOS activity in proximal vagina, estrogens are known to enhance vaginal blood flow. This paradoxical observation may be explained by differential regulation of n-NOS and e-NOS in the proximal and distal vagina. We suggest that changes in vaginal blood flow and compliance may depend on the endocrine status and the levels of circulating androgens and estrogens.

The regulatory role of nitric oxide (NO) in vaginal perfusion remains unclear. We used specific inhibitors of enzymes in the NO-cyclic GMP (NO-cGMP) pathway and investigated their effects on vaginal blood flow in the rabbit. NO synthase (NOS) activity was similar in both the proximal and distal rabbit vagina; whereas, arginase activity was 3.4-fold higher in the distal vagina. Intravenous administration of the NOS inhibitor L-NAME resulted in a 66% reduction in genital tissue oxyhemoglobin and a 53% reduction in vaginal blood flow. This attenuation occurred despite a 20-30% increase in systemic arterial pressure. The arginase inhibitor ABH caused a 2.1-fold increase in genital tissue oxyhemoglobin and 34% increase in vaginal blood flow. The guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one and the phosphodiesterase type 5 inhibitor sildenafil caused in a 37% reduction and a 44% increase in vaginal blood flow, respectively. These observations suggest that the NO-cGMP pathway is an important regulator of vaginal hemodynamics.