雄激素与勃起功能障碍

雄激素对维持性欲是必不可少的,它通过中枢和外周两个层面,以多种机制控制着阴茎勃起的启动、维持和终结.雄激素缺乏不但导致性欲减退,还可造成阴茎的组织结构损害及勃起相关活性物质发生明显改变,如阴茎海绵体平滑肌含量减少、结缔组织增多及白膜下脂肪细胞沉积等.阴茎勃起时,海绵体组织的上述改变可致静脉闭塞不全而发生静脉漏,出现勃起功能障碍(ED).对性腺功能减退的ED患者补充睾酮可收到良好的治疗效果.睾酮替代治疗期间需密切观察,避免不良反应的发生.     

阴茎脚白膜折叠+背深静脉包埋术治疗中重度静脉性勃起功能障碍

目的 探讨阴茎脚白膜折叠+背深静脉包埋术治疗中重度静脉性勃起功能障碍的疗效.方法 21例中重度静脉性勃起功能障碍患者接受阴茎脚白膜折叠+背深静脉包埋术,在其术前和术后12个月分别作心理评估(症状自评量表,SCL90)、勃起功能评分(勃起功能国际问卷-5,IIEF-5评分)及勃起硬度检测(即时阴茎勃起硬度监测,口服西地那非片100 mg 30 min后予视听性刺激+Rigiscan监测阴茎勃起硬度),对比术前、术后上述评估指标变化,并用统计软件(SPSS-13.0)对结果进行统计学分析,判断其手术后疗效.结果 21例患者完成了术后1 2个月的随访,其中1 7例“显效”,4例“有效”,“显效率”为8 1％;术后IIEF-5评分、即时阴茎勃起硬度值同术前相比,差异有统计学意义(P＜0.001).结论 阴茎脚白膜折叠+背深静脉包埋术通过“疏导”阴茎静脉血流回流,增加阴茎静脉回流的阻力,能显著改善阴茎勃起功能,术后随访中期效果满意,远期效果值得期待.     

通过长期服用西地那非治疗大鼠因阴茎组织纤维化引起的勃起功能障碍

因阴茎组织纤维化引起的勃起功能障碍特点是:血管平滑肌细胞(SMC)凋亡,阴茎海绵体纤维化,海绵体静脉闭塞功能障碍(CVOD)。PDE5抑制剂可通过上调诱生型一氧化氮合酶(NOS2A)来抑制阴茎     

NADPH氧化酶与男性勃起功能障碍

勃起功能障碍是男性的常见病和多发病。目前认为氧化应激是引起阴茎勃起功能障碍的重要机制之一。NADPH氧化酶广泛存在于机体多个系统(包括阴茎组织),发挥重要的生理功能。在多种病理情况下,NADPH氧化酶可以在阴茎组织中催化合成大量活性氧,导致过度氧化应激,从而影响阴茎勃起功能。本文就NADPH氧化酶的组成、同源物、活性调节、生理功能、在勃起功能障碍中的作用以及在勃起功能障碍治疗中的应用作一综述。     

阴茎海绵体内压测定技术在阴茎勃起功能障碍动物模型中的应用

阴茎勃起是一类血管神经事件,其主要依靠海绵体平滑肌细胞的舒张,海绵体窦内充血肿胀,压迫白膜下静脉丛造成静脉阻塞,阴茎海绵体内压增高,阴茎疲软时海绵体窦内压力值约5~7 mmHg,而达到完全勃起状态时窦内压力可达到100 mmHg以上。动物阴茎勃起功能障碍模型研究中,海绵体内压测定是判断阴茎勃起功能的金标准。近年来国外已有学者成功应用遥测技术监测大鼠阴茎海绵体内压变化,而国内仍未见相关报道。本文就动物勃起功能障碍模型阴茎海绵体内压测定技术的发展做一简要综述。     

安特尔对糖尿病患者阴茎勃起功能障碍的影响

目的:探讨安特尔治疗糖尿病患者阴茎勃起功能障碍的效果。方法:将80例阴茎勃起功能障碍、且经万艾可治疗无效的2型糖尿病患者,随机分为两组。安万组:40 例,在用万艾可治疗的同时加用安特尔(120mg/d);维万组:40例,在用万艾可治疗的同时加用维生素E(30 mg/d)。两组均治疗1 个月,观察患者治疗前后血清睾酮水平、IIEF 5评分和阴茎海绵体血流量的变化。结果:安万组较治疗前血清睾酮明显升高(P<0.01),IIEF 5评分显著提高(P<0.05),阴茎海绵体血流量明显增加(P<0.05);其中30例(75%)患者性交时阴茎能满意地勃起;未出现任何不良反应。维万组治疗前后上述指标无明显变化(均P>0.05)。结论:安特尔能显著改善经用万艾可治疗无效的糖尿病患者的阴茎勃起功能,且安全性好。     

阴茎勃起功能障碍的彩色多普勒超声评估

阴茎勃起是在神经系统支配下阴茎小动脉扩张，海绵窦充血，静脉关闭的复杂血流动力学变化过程，其中任何一个环节失调都会导致勃起功能障碍(erectile dysfunction，ED)，即阴茎持续不能达到或维持充分勃起以获得满意的性生活。阴茎血管造影术(Angiography)和阴茎海绵体造影术(Cavemosography)是评价阴茎血管功能的传统方法，     

硫化氢与阴茎勃起功能关系研究进展

硫化氢(H2S)是继NO和CO之后第3种被发现的具有内源性活性的气体信号分子,在哺乳动物体内H2S主要由两种蛋白酶———胱硫醚-β-合酶(CBS)和胱硫醚-γ-裂合酶(CSE)合成产生。H2S在体内具有重要的生理调节功能,它可作用于ATP敏感性钾离子通道(K+-ATP)舒张血管平滑肌,与睾酮及NO协同作用舒张阴茎海绵体平滑肌,促进阴茎勃起等。目前,治疗勃起功能障碍(ED)主要应用选择性的5-型磷酸二酯酶(PDE5)抑制剂,而临床发现PDE5抑制剂对部分ED患者治疗无效,因此,进一步研究H2S在阴茎勃起过程中的调节机制及作用,可能为ED提供了新的治疗途径。     

脂肪源性干细胞治疗勃起功能障碍的研究进展

勃起功能障碍(erectile dysfunction,ED)是男性常见疾病,直接影响患者的生活质量.近年来,人们对阴茎勃起机制和ED病理生理学的研究取得一定进展,有了许多治疗ED的方法,如:口服磷酸二酯酶5型(phosphodiesterase 5,PDE5)抑制剂、阴茎海绵体内注射血管活性药物及阴茎假体植入[1]等.     

保护阴茎血管内皮功能:勃起功能障碍治疗新途径

阴茎勃起是典型的神经血管过程。越来越多证据表明,阴茎血管内皮功能异常是勃起功能障碍发生的重要机制。保护阴茎血管内皮功能可以改善勃起功能,血管内皮保护剂通过减轻氧化应激损伤、保护勃起递质的功能活性,改善阴茎海绵体血管内皮功能,从而治疗勃起功能障碍。保护阴茎血管内皮功能,将成为勃起功能障碍治疗的新途径。     

New concept parameters of RigiScan in differentiation of vascular erectile dysfunction: Is it a useful test?

BACKGROUND: The aim of this study is to investigate the value of new nocturnal penile tumescence recording parameters, such as tumescence activity unit and rigidity activity unit values, total erection number and erection times, in differentiating between psychogenic erectile dysfunction and organic erectile dysfunction. We also aimed to determine the role of these parameters in differentiating arterial erectile dysfunction from veno-occlusive dysfunction. METHODS: Eighty-seven consecutive patients were allocated into three groups as psychogenic, arterial and venous erectile dysfunction after investigations. Nocturnal penile tumescence recording parameters between psychogenic and vascular erectile dysfunction and arterial and veno-occlusive dysfunction were compared. Mann-Whitney U-test, Pearson's chi2 test and correlation coefficient tests were used for statistical analysis. RESULTS: Depending on intracavernous injection, penile Doppler ultrasonography and cavernosometry tests, 37 patients (43%) had psychogenic impotence while 50 (57%) had organic pathologies. Of the 50 patients diagnosed with vascular impotence, 29 (48%) had arterial failure and 21 (42%) had veno-occlusive dysfunction. Nocturnal penile tumescence recording revealed psychogenic erectile dysfunction in 34 patients (39%) and vascular erectile dysfunction in 53 patients (61%). Nocturnal penile tumescence recording has been regarded as the gold standard and, in our series, it showed 90.6% sensitivity and 88.2% specificity in differentiating the cause of erectile dysfunction. Values of rigidity activity unit and tumescence activity unit were significantly higher in patients with psychogenic impotence (P < 0.001), when compared with vascular impotence. In patients with a vascular cause, no difference was found between arterial failure and veno-occlusive dysfunction with regard to tip tumescence activity unit, base tumescence activity unit, tip rigidity activity unit, base rigidity activity unit and erection time (P > 0.001). However, patients with arterial failure had less erection than patients with veno-occlusive dysfunction (P < 0.001). CONCLUSION: New recording parameters of nocturnal penile tumescence can differentiate organic and psychogenic erectile dysfunction more precisely. However, these recording parameters cannot distinguish subgroups with a vascular cause of erectile dysfunction.     

Novel nitric oxide signaling mechanisms regulate the erectile response

Nitric oxide (NO) is a physiologic signal essential to penile erection, and disorders that reduce NO synthesis or release in the erectile tissue are commonly associated with erectile dysfunction. NO synthase (NOS) catalyzes production of NO from L-arginine. While both constitutively expressed neuronal NOS (nNOS) and endothelial NOS (eNOS) isoforms mediate penile erection, nNOS is widely perceived to predominate in this role. Demonstration that blood-flow-dependent generation of NO involves phosphorylative activation of penile eNOS challenges conventional understanding of NO-dependent erectile mechanisms. Regulation of erectile function may not be mediated exclusively by neurally derived NO: Blood-flow-induced fluid shear stress in the penile vasculature stimulates phosphatidyl-inositol 3-kinase to phosphorylate protein kinase B, which in turn phosphorylates eNOS to generate NO. Thus, nNOS may initiate cavernosal tissue relaxation, while activated eNOS may facilitate attainment and maintenance of full erection.     

The effects of androgen on penile reflex, erectile response to electrical stimulation and penile NOS activity in the rat

Aim: To investigate the effects of androgen on penile erection through the reflex arc and penile corpus cavernosum,and study the respective roles of testosterone (T) and dihydrotestosterone (DHT) in penile erection ira rats. Methods:Male Sprague-Dawley rats were castrated and implanted with silastic brand silicone tube containing T or DHT, with orwithout daily injections of a 5a-reductase inhibitor, MKM-434. The penile reflex, erectile response to electrical stimula-tion (ES) of the cavernous nerves and penile nitric-oxide synthase (NOS) activity were observed under varying andro-genic status. Results: Penile reflex erection in the rat was, on the whole, related to serum T levels though the numberof glans engorgernents was not. The number of cups and flips was significantly decreased by castration, and restoredto the control level by T supplementation. Erectile response to ES and NOS activity in penile tissue was also related toserum T level. T administered together with a ,5a-reductase inhibitor no longer restored the number of reflex erection,erectile responses to ES and NOS activity in the corpus cavemosum. Conclusion: Androgen influenced the penile re-flex arc, corpus cavemosum, and the perinea] striated muscles, ha reflex erection, erectile response to ES and penileNOS activity in the rat, T seeras to be first conyerted to DHT, the more active androgen modality. (Asian JAndrol1999Dec; 1: 169-174)     

Effects of transanal pelvic plexus stimulation on penile erection: clinical implications

Objective To determine the ability of transanal pelvic plexus stimulation (TPPS) in inducing penile tumescence in patients with non-neurogenic erectile dysfunction (ED) and to compare the erection degree with papaverine-induced erection. Patients and methods The cavernous electrical activity (CEA) in 21 men with non-neurogenic erectile dysfunction was measured during TPPS by electromyography of corpus cavernosum and the erection degree of penis (flaccid, semi-rigid, rigid) was noted. The stimulation amplitude was increased from 20 to 100 mA. All patients also underwent intracavernous papaverine injection and further CEA recordings were obtained. Results Twelve and nine patients were diagnosed with vasculogenic (VED) and non-vasculogenic ED (NVED), respectively. TPSS led to a penile erectile response in 12 patients (57%), whereas papaverine injection caused erection in 16 (76.2%) patients. The mean baseline CEA (16.9 ± 9.1 mV) did not change with TPPS, but papaverine significantly decreased the mean CEA to 12.3 ± 4.9 mV (P < 0.001). CEA recordings of 16 (76.2%) patients revealed a significant decrease after papaverine injection, however seven (33.3%) patients showed significant CEA decrease in response to TPPS. Both TPPS and papaverine were observed to have a higher effect in patients with NVED in terms of inducing penile erection and decreasing CEA compared to their effects in patients with VED. Conclusion TPPS induces penile erection and decreases CEA for some extent, but to a lesser degree compared to papaverine. As further improvements are achieved in the methodology of TPPS, it may be a valuable method in the evaluation patients with erectile dysfunction.     

Central control of erection and its pharmacological modification

Advances in our understanding of the local mechanisms of penile erection have paralleled the use of pharmacological treatments of erectile dysfunction. In contrast, the spinal and supraspinal mechanisms that control penile erection are less well understood. Although the role of hypothalamic areas (medial preoptic area, paraventricular nucleus) and brainstem nuclei (raphe nuclei) in penile erection has been evaluated, as has the role of an association between neuromediators and receptors (serotonin, dopamine, noradrenalin, glutamate, gamma-aminobutyric acid, nitric oxide), an integrative view of the central mechanisms of penile erection is lacking. New strategies to treat erectile dysfunction employ oral agents, some of which target central brain nuclei. The future of such treatments largely depends on a better understanding of the central mechanisms of penile erection.     

Surgical management of erectile dysfunction

The introduction of penile prosthesis in the early 1970s has been the first breakthrough in the treatment of erectile dysfunction. Since then a variety of treatment options for erectile dysfunction have been developed, including penile vascular surgery, injection therapy, vacuum erection device therapy, intraurethral and oral pharmacotherapy. Although the percentage of men newly diagnosed with erectile dysfunction who undergo surgical treatment has declined, the number of men presenting with erectile dysfunction continues to increase out of proportion to this decline. Moreover, many men that are now effectively managed with medical treatment are likely to require penile prosthesis implantation as their erectile dysfunction progresses. This chapter will focus on the surgical management of erectile dysfunction and in particular on penile prosthesis implantation.     

Erectile dysfunction in hypertensive men: sleep-related erections, penile blood flow and musculovascular events

To explore how hypertension affects penile erection, we studied erectile hemodynamics during nocturnal penile tumescence in 3 groups of middle-aged men: hypertensive patients with and without erectile dysfunction, and normotensive controls without erectile problems. The hypertensive patients were not taking antihypertensive medication. Evaluations included standard monitoring of penile circumference change as well as noninvasive monitoring of penile segmental pulsatile blood flow and activity in the bulbocavernosus-ischiocavernosus muscles. Variables differed in how they discriminated among groups. Median amplitude of penile blood flow during rapid eye movement sleep differed significantly among all 3 study groups: controls had the highest amplitudes, patients without erectile problems had lower values and patients with erectile complaints had the lowest values. By contrast, standard measures of nocturnal penile tumescence (that is based on penile circumference change during sleep) only distinguished the patients with erectile problems from the 2 other groups. Density of musculovascular event clusters during rapid eye movement sleep (nearly simultaneous muscle activity burst, blood flow burst and circumference pulsation) distinguished the 2 groups of hypertensive men from controls. The sensitivity of the blood flow measure to changes in the hypertensive men without erectile complaints may indicate that the measure can reveal subclinical signs of developing vasculogenic erectile dysfunction.     

Intracavernous pharmacotherapy

Summary Intracavernous application of vasoactive substances not only has enhanced our understanding of penile hemodynamics, the physiology of penile erection, and the pathophysiology of erectile dysfunction but also has revolutionized the diagnosis and treatment of erectile dysfunction in the last 15 years. Virag was the first to report on the erectile effect of papaverine in humans, and Brindley later reported the effect of intracavernous application of alpha-receptor-blocking agents on cavernous tissue. These reports led to numerous basic and clinical investigations and ultimately established a new treatment alternative for patients with erectile dysfunction that is now considered to be the treatment of choice for most patients. Changes in penile hemodynamics include the relaxation of cavernous smooth musculature and arteries, which leads to an increase in arterial blood flow and a restriction of venous outflow through a compression of subtunical veins. These hemodynamic changes are the prerequisite for the induction and maintenance of penile erection. With the intracavernous application of vasoactive substances it was possible to influence penile hemodynamics at a local level and to induce an erection despite alterations in the nervous system, penile arterial blood flow, cavernous musculature, or neurotransmitter status. In addition, the localapplication of pharmacologically active substances directly to the end organ enabled the achievement of high local drug concentrations without severe systemic side effects. The commonly used substances are papaverine, the combination of papaverine and phentolamine, and prostaglandin E1 (alprostadil). In addition to these established substances, several other regimens, such as linsidomine (SIN-1), calcitonin gene-related peptide (CGRP), moxisylyte, and various triple- or quadruple drug mixtures have been described. In addition, several other compounds as well as different routes of administration are on the horizon and may prove to be effective in the future diagnosis and treatment of erectile dysfunction.     

Pathophysiology of Erectile Dysfunction

Physiology of erection and pathophysiology erectile dysfunction is reviewed. Analysis is obtained from basic and clinical research including animals studies, anatomical studies, and molecular and cellular research on corporal tissue obtained during penile prosthesis implantation. Supraspinal influences and spinal influence on penile erection has been learned from spinal cord injury patient. Corporal smooth muscle relaxation of penile arteries and corpus cavernosum leads to penile erection, results from parasympathetic/nonadrenergic noncholinergic neural pathway activation and simultaneous inhibition of sympathetic outflow. Anatomical studies taught understanding of the mechanism for restriction of blood outflow from the corpora cavernosa. The change of smooth muscle tone has emerged as a key factor in erection and detumescence. Many independent factors converge on the modulation of corporal smooth muscle tone. Neuronal and local neurotransmitter effects via gap junction, potassium channels, and calcium channel. A nitric oxide/cyclic guanosine monophosphate mechanism as well as cyclic aminomonophosphate has an important role in mediating the corporal smooth muscle relaxation necessary for erectile function. Erectile dysfunction can be due to vasculogenic, neurogenic, hormonal, veno-occlusive, psychogenic and/or pharmacogenic factors as well as alterations in the nitric oxide/cyclic guanosine monophosphate (cGMP) or cyclic aminophosphate (cAMP) pathway or other regulatory mechanisms including gap junction or ionic channel resulting in an imbalance in corporal smooth muscle contraction and relaxation. Our present knowledge of the hemodynamics, functional anatomy, neurophysiology, and neuropharmacology of penile erection and dysfunction at the cellular and molecular level has led to better understanding of physiology and pathophysiology of erectile dysfunction.     

Iatrogenic causes of erectile dysfunction

Normal penile erection is a complex event dependent upon the proper sequential function of the endocrine, nervous, and vascular systems. Medical or surgical therapy can influence those systems and so cause erectile dysfunction. Physicians must understand these iatrogenic causes of erectile dysfunction in order to prevent or reverse them.