帕金森病的尿动力学表现及临床意义

为了评估有持久膀胱排尿障碍的帕金森氏病患者的尿动力学表现及其临床意义,对25例帕金森氏病患者行尿动力检查,并要求记录并回收24小时排尿日记.结果显示,1)有18例患者出现膀胱过度活动,逼尿肌收缩力低下或无反射4例,膀胱出口梗阻6例,另3例检查结果正常,无一例出现逼尿肌-括约肌协同失调; 2)患者所返回的排尿日记显示帕金森氏病患者普遍出现日排尿次数增加及每次排尿量的减少.由此可以得出结论:逼尿肌反射亢进是帕金森氏病患者尿动力学检查的最常见类型;尿动力学检查对正确处理帕金森氏病患者的排尿障碍有指导意义.     

慢性非细菌性前列腺炎/慢性骨盆疼痛综合征患者的尿动力学检查

目的:探讨尿动力学检查在了解慢性非细菌性前列腺炎/慢性骨盆疼痛综合征(Chronicabacterialprostatitis/chronicpelvicpain syndrome,CPPS)患者中下尿路症状(LUTS)产生原因的作用。方法:对36例难治性慢性前列腺炎/盆腔疼痛综合征患者行尿流动力学压力-流率测定,同步测定膀胱压、逼尿肌压、同步肌电图测定,了解其症状产生的原因。结果:36例患者中,尿动力学证实膀胱出口梗阻14例(39%);逼尿肌过度活动者8例,其中有7例与BOO同时存在;假性逼尿肌尿道外括约肌协同失调6例(16.7%);逼尿肌收缩力低下者5例(13.9%)。结论:对难治性CPPS患者进行尿动力学检查有助于对此类患者LUTS产生的原因进行鉴别,从而可以采取有针对性的治疗。     

动态尿动力学评价前列腺增生合并肾积水、肾功能损害可复性临床应用

目的:探讨术前、术后尿动力学检测及其对合并肾积水、肾功能损害的临床意叉.方法:膀胱出口梗阻≥Ⅲ度的BPH患者按是否合并肾积水、肾功能损害分为两组,即无合并症的A组198例,有合并症的A组48例,记录术前、术后2次影像、尿动力学、肾功能等检查结果,对A、B组间和B组术前、术后结果进行比较分析.结果:(1)术前合并低顺应性膀胱(low compliance bladder LCB),膀胱逼尿肌括约肌协同失调(detrusor sphincter dyssynergia DSD),逼尿肌活动亢进(detrusor overactivity DO)的患者,A、B组分别18.2%、29.3%、29.3%和83.3%、54.2%、14.6%,不稳定膀胱(detrusor instability DI)、膀胱逼尿肌收缩功能损害(detrusor contractile functional lesion IDC)早期、IDC中晚期的患者,A、B组分别为128例、39例、6例和19例、18例、8例(P＜0.01);(2)A、B组间术前、术后DI、IDC早期、尿动力学残余尿量(residual urine RU)、充盈期膀胱压力(filling phase dertusor pressure FPPdet)、排尿期膀胱压力(utination phrase dertusor pressure UPPdet)最大尿流率(maximum flow rate MFR)差异有显著性(P＜0.05).(3)术前、术后3个月B组IDC中晚期尿动力学参数有变化,大多仍未能恢复,高顺应性膀胱(High compliance bladder HCB)尿动力学参数差异无统计学意义(P＞0.05).结论:BPH无合并肾积水、肾功能损害患者,应争取在PCB前手术,可避免肾并发症发生;合并肾积水、肾功能损害,争取在IDC早期前,或者PCB合并其他膀胱功能改变前手术,有助于肾积水、肾功能损害的恢复;如已是IDC晚期及HCP的患者,则肾积水、肾功能损害3个月内恢复效果较差.     

脑桥上中枢损伤与腰骶段脊髓损伤患者的膀胱功能障碍及尿动力特点研究

目的:比较脑桥以上中枢损伤与腰骶段脊髓损伤患者的膀胱功能障碍及尿动力学特点。方法:回顾性分析2011年3月至2014年5月我院收治的78例中枢神经损伤患者的临床资料,包括临床表现、诊断、排尿方式、残余尿、尿动力学检查结果。其中,脑桥以上中枢损伤组43例,腰骶段脊髓损伤组35例,分析和比较两组患者的自由尿流率参数和完全膀胱测压参数。结果:两组间的最大尿流率、排尿量比较差异无统计学意义(P0.05),脑桥上中枢损伤组的残余尿量明显低于腰骶段脊髓损伤组,差异有统计学意义(P0.05)。与腰骶段脊髓损伤组比较,脑桥以上损伤组的膀胱容量明显减少,最大尿流率时的压力、逼尿肌的最大压力及平均压力明显增加,差异均有统计学意义(P0.05)。两组膀胱的顺应性、逼尿肌稳定性比较差异有统计学意义(P0.05),脑桥以上中枢损伤患者的多数表现为低顺应性膀胱(27/43),胸腰段脊髓损伤患者主要表现为高顺应性膀胱(21/35);脑桥以上损伤组多表现为逼尿肌的过度活动(29/43),而腰骶段脊髓损伤组更多表现为逼尿肌的无反射和弱反射(20/35)。结论:脑桥以上损伤患者主要表现为逼尿肌过度活动和膀胱容量的显著降低,以低顺应性膀胱为主;腰骶段脊髓损伤患者的逼尿肌多为无反射和弱反射,以高顺应性膀胱为主。     

慢性非细菌性前列腺炎／慢性骨盆疼痛综合征患者的尿动力学检查

目的：探讨尿动力学检查在了解慢性非细菌性前列腺炎／慢性骨盆疼痛综合征 （Chronic abacterial prostatitis/chronic pelvic pain syndrome, CPPS） 患者中下尿路症状（LUTS）产生原因的作用。方法：对36例难治胜慢性前列腺炎／盆腔疼痛综合征患者行尿流动力学压力-流率测定,同步测定膀胱压、逼尿肌压、同步肌电图测定,了解其症状产生的原因。结果：36例患者中,尿动力学证实膀胱出口梗阻14例（39％）;逼尿肌过度活动者8例,其中有7例与BOO同时存在;假性逼尿肌尿道外括约肌协同失调6例（16．7％）;逼尿肌收缩力低下者5例（13．9％）。结论：对难治性CPPS患者进行尿动力学检查有助于对此类患者LUTS产生的原因进行鉴别。从而可以采取有针对性的治疗。     

大鼠逼尿肌不稳定模型的建立及逼尿肌T型钙通道亚型表达的初步研究

目的:建立膀胱逼尿肌不稳定的大鼠模型并初步研究逼尿肌T型钙通道亚型的表达。方法:以增加膀胱出口梗阻的方法诱导膀胱逼尿肌不稳定的出现;以RT-PCR的方法检测正常膀胱和不稳定膀胱逼尿肌上T通道亚型的表达。结果:梗阻后5、6周逼尿肌不稳定发生率高且稳定;不稳定逼尿肌细胞与正常逼尿肌细胞均有α1I亚型表达且无数量差异,逼尿肌细胞有α1G亚型的表达,而正常逼尿肌上无此亚型表达。结论:梗阻第5、6周的动物是用来研究DI产生机制的良好模型;α1G亚型可能与逼尿肌不稳定的发生具有一定关系。     

前列腺增生伴Ⅱ型糖尿病患者的尿流动力学分析

目的:探讨前列腺增生伴Ⅱ型糖尿病患者的尿流动力学改变,并对该类患者提出合理的治疗和处理。方法:选取从2010年9月~2013年9月在本院泌尿外科一病房行经尿道前列腺电切,术后病理诊断为前列腺增生术前行尿流动力学检查的患者349例,分为单纯前列腺增生组158例(对照组)及前列腺增生合并Ⅱ型糖尿病组191例(研究组),前列腺增生合并Ⅱ型糖尿病组又分为两个亚组,即空腹血糖≤6.1 mmol/L组(亚1组)96例及空腹血糖6.1 mmol/L组95例(亚2组)。比较各组患者尿流动力学各项检查结果。结果:1)、比较亚2组和对照组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,P值均0.05。2)、亚1组和对照组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,除亚1组病程5年的残余尿量、顺应性P值0.05外,其他均0.05。3)、亚1组和亚2组患者残余尿量、最大尿流率、最大尿流率时逼尿肌压、最大逼尿肌压及顺应性,P值均0.05。4)、亚1组和亚2组不稳定膀胱率明显高于对照组。结论:Ⅱ型糖尿病能加重前列腺增生患者膀胱功能障碍,及早控制血糖能减轻、延缓膀胱功能障碍。     

低频电刺激联合间歇导尿及Motomed运动训练对脊髓损伤致神经源性膀胱患者膀胱内压力及膀胱容量的影响

目的:探讨低频电刺激联合间歇导尿及Motomed运动训练对脊髓损伤致神经源性膀胱患者膀胱内压力及膀胱容量的影响。方法:选取我院2015年12月～2018年2月收治的脊髓损伤致神经源性膀胱患者92例,根据随机数字表法将其分为对照组(n=46)与研究组(n=46)。两组均给予间歇性导尿、盆底肌训练、膀胱功能训练等常规干预,对照组在此基础上采取低频电刺激,研究组于对照组基础上采取Motomed运动训练,两组均干预2个月。比较两组的临床疗效、治疗前及治疗2个月后的排尿情况(日均单次排尿量、日单次最大排尿量、日均排尿次数)、尿动力学情况(最大尿流率、膀胱容量、残余尿量、膀胱内压力)、LUTS(国际下尿路症状评分)及USDS(泌尿症状困扰评分)。结果:治疗后,研究组总有效率(93.48%)显著高于对照组(78.26%)(P0.05);治疗2个月后,两组日均单次排尿量、日单次最大排尿量、日均排尿次数、最大尿流率、膀胱容量、膀胱内压力均较治疗前显著增多,且研究组以上指标均明显高于对照组(P0.05);两组LUTS及USDS分值均较治疗前显著降低,且研究组以上指标均显著低于对照组(P0.05)。结论:间歇导尿联合低频电刺激与Motomed运动训练可有效改善脊髓损伤致神经源性膀胱患者尿动力学状态及排尿情况,增大膀胱容量及膀胱内压力等,缓解下尿路症状及泌尿症状困扰程度,提高治疗效果。     

臭氧水膀胱腔内灌注治疗女性膀胱过度活动症疗效评价*

目的:评价臭氧水膀胱腔内灌注疗法对膀胱过度活动症的有效性和安全性。方法:2016年1月至2016年12月间共60例患者入组,所有患者均行尿流动力学检查证实膀胱逼尿肌不稳定。患者被随机分入治疗组(n=30)和对照组(n=30),对照组采用行为训练疗法并口服索利那新治疗。治疗组在行为训练疗法于口服索利那新的基础上,同时行臭氧水膀胱腔内灌注治疗。在治疗结束时通过患者病情改善情况评价疗效,主要评价指标包括:治疗前、后的患者24h排尿次数、平均夜尿次数、24h尿失禁次数、OABSS评分、I-QOL评分、治疗前和治疗结束末4周复查尿流动力学检查评估,并评估患者的不良反应。获得的数据采用t检验进行统计学分析。结果:结果证实,在24h排尿次数、平均夜尿次数、OABSS评分和I-QOL评分方面,各组治疗后有改善,而臭氧治疗组改善情况优于对照组(P0.05)。尿流动力学检查证实所有治疗后患者逼尿肌不稳定情况均有改善;初始尿意时膀胱容量、最大膀胱容量、储尿期膀胱逼尿肌最大压力变化情况治疗组改善优于对照组。不良反应由患者自主报告,治疗组主要表现为灌注后尿道内及下腹部不适感,多自主恢复,两组间差异不明显(P0.05)。结论:臭氧水膀胱腔内灌注治疗女性膀胱过度活动症安全、有效,能改善膀胱过度活动症患者排尿次数、夜尿次数和24小时尿失禁次数,能改善OABSS评分,能改善尿流动力学结果,提高患者的生活质量。     

TURP联合经尿道膀胱颈切开术治疗小体积前列腺增生所致膀胱出口梗阻的疗效分析

目的:探讨经尿道前列腺电切术(TURP)联合经尿道膀胱颈切开术(TUIBN)治疗小体积前列腺增生(BPH)所致膀胱出口梗阻的疗效。方法:选择2009年1月~2013年12月我院收治的小体积BPH患者,其中单纯经尿道前列腺电切术(TURP组)48例,经尿道前列腺电切术联合经尿道膀胱颈切开术(TURP+TUIBN组)48例。比较两组的术前、术后国际前列腺症状评分(IPSS)、残余尿量(PVR)、最大尿流率(Qmax)等,以及术后并发症的发生情况。结果:TURP+TUIBN组术中出血量较TURP组明显增多(P0.05),两组手术时间、组织切除质量比较,差异均无统计学意义(P0.05);与TURP组比较,TURP+TUIBN组术后6个月IPSS评分、PVR明显下降,Qmax、膀胱压力明显上升(P0.05);TURP+TUIBN组并发症发生率为4.2%,显著低于TURP组16.7%(P0.05)。结论:TURP+TUIBN治疗小体积前BPH所致膀胱出口梗阻,可彻底切除增生腺体,消除小体积BPH的各种梗阻因素,减少术后膀胱颈挛缩的发生。     

Behavioural treatment of urinary incontinence in geriatric patients.

Urinary incontinence and a program to treat it were studied in a geriatric hospital. Of 161 men, 58 (36%) were incontinent. The most common probable causes were cerebrovascular accident and organic brain syndrome. Evaluation by cystometry (after treatment of infections) in 30 patients showed 24 (80%) to have detrusor hyperreflexia. Twenty patients with hyperreflexia completed a timed-voiding routine, which benefited 17 of them (85%).     

Is There a Role for alpha-Blockers for the Treatment of Voiding Dysfunction Unrelated to Benign Prostatic Hyperplasia?

alpha-Adrenoreceptor antagonists have become the primary medical treatment for lower urinary tract symptoms associated with benign prostatic hyperplasia (BPH). It was presumed that the primary mechanism by which alpha-blockers reduced lower urinary tract symptoms (LUTS) was by relaxation of smooth muscle in the prostate through a sympathetic response. Reduction of outlet resistance leads to changes in bladder function, thus improving both storage and voiding symptoms. However, it was observed that many patients with BPH-associated LUTS had significant improvement in storage symptoms without subjective or objective improvement in voiding. Storage symptoms associated with detrusor overactivity (frequency, urgency, and urge incontinence) are typically thought of as being parasympathetically mediated, and therefore anticholinergic medications have been the mainstay of pharmacological treatment, but recent work has suggested that several nonparasympathetic-mediated mechanisms may cause detrusor overactivity. Because alpha receptors appear to play a role in lower urinary tract function at multiple sites and levels, alpha-blockers could be used to treat voiding dysfunction not related to BPH. In addition, these nonprostate effects should be gender-independent, making the use of alpha-blockers plausible in women with specific types of voiding dysfunction.     

Detrusor expulsive strength is preserved, but responsiveness to bladder filling and urinary sensitivity is diminished in the aging mouse

The prevalence of urinary symptoms increases with age and is a significant source of distress, morbidity, and expense in the elderly. Recent evidence suggests that symptoms in the aged may result from sensory dysfunction, rather than abnormalities of detrusor performance. Therefore, we employed a pressure/flow multichannel urethane-anesthetized mouse cystometry model to test the hypothesis that in vivo detrusor performance does not degrade with aging. Secondarily, we sought to evaluate sensory responsiveness to volume using pressure-volume data generated during bladder filling. Cystometric data from 2-, 12-, 22-, and 26-mo-old female C57BL6 mice were compared. All 2- and 12-mo-old mice, 66% of 22-mo-old mice, and 50% of 26-mo-old mice responded to continuous bladder filling with periodic reflex voiding. Abdominal wall contraction with voiding had a minimal contribution to expulsive pressure, whereas compliance pressure was a significant contributor. Maximum bladder pressure, estimated detrusor pressure, detrusor impulse (pressure-time integral), as well as indices of detrusor power and work, did not decrease with aging. Bladder precontraction pressures decreased, compliance increased, and nonvoiding contraction counts did not change with increasing age. Intervoid intervals, per-void volumes, and voiding flow rates increased with age. Calculations approximating wall stress during filling suggested loss of bladder volume sensitivity with increasing age. We conclude that aging is associated with an impaired ability to respond to the challenge of continuous bladder filling with cyclic voiding, yet among responsive animals, voiding detrusor contraction strength does not degrade with aging in this murine model. Furthermore, indirect measures suggest that bladder volume sensitivity is diminished. Thus, changes in homeostatic reserve and peripheral and/or central sensory mechanisms may be important contributors to aging-associated changes in bladder function.     

The influence of ovariectomy and estrogen replacement on voiding patterns and detrusor muscarinic receptor affinity in the rat

A rat model of ovariectomy-induced voiding dysfunction was established and the effects of ovariectomy and subsequent estrogen replacement on the affinity of muscarinic receptors in the rat bladder were determined. Voiding frequency and spatial distribution patterns were documented in sham-operated (control), and ovariectomized (placebo- or estrogen-treated) rats. The ovariectomized rats had a significantly different urinating pattern, i.e. higher voiding frequency and less peripheral voiding than the sham-operated group, suggestive of urge incontinence. Using this model of voiding dysfunction, negative logs of dissociation constants of carbachol of the rat detrusor muscarinic receptors were then determined indirectly using the Furchgott's double-reciprocal method. Receptor affinities were not significantly different in all groups compared to control females. In conclusion, a model of ovariectomy-induced voiding dysfunction in ovariectomized rats was established, where bladder dysfunction occurred with no significant changes in the affinity of muscarinic receptors.     

Vascular response of the rabbit bladder to chronic partial outlet obstruction

Partial outlet obstruction of the rabbit urinary bladder results, initially, in a rapid increase in bladder mass and remodeling of the bladder wall. Previously, it was shown that this response was characterized by serosal growth (thickening) which was apparent after 1 day of obstruction, before any visible vascularization was observed. After 1 week of obstruction, significant microvessel formation was seen in the transition region between the detrusor smooth muscle and the thickening serosa; after 2 weeks the entire serosa was vascularized.In this study we investigated the effect of chronic (4 week) partial outlet obstruction on microvessel density and distribution in the bladder wall immunohistochemically using CD31 as a marker for vascular endothelium. Transverse sections of bladder wall were examined after 4 weeks of no surgery, sham surgery or partial obstruction.The microvessel density of the obstructed rabbit bladder mucosa and detrusor smooth muscle increased relative to augmentation of these compartments while new vessels appeared in the thickening serosa. Although vessel density did not change with obstruction a significant shift in mean vessel circumference to the left occurred indicating a significant increase in the number of microvessels and small vessels consistent with angiogenesis.     

Alteration in expression of myosin isoforms in detrusor smooth muscle following bladder outlet obstruction

Partial urinary bladder outlet obstruction (PBOO) in men, secondary to benign prostatic hyperplasia, induces detrusor smooth muscle (DSM) hypertrophy. However, despite DSM hypertrophy, some bladders become severely dysfunctional (decompensated). Using a rabbit model of PBOO, we found that although DSM from sham-operated bladders expressed nearly 100% of both the smooth muscle myosin heavy chain isoform SM-B and essential light chain isoform LC_17a, DSM from severely dysfunctional bladders expressed as much as 75% SM-A and 40% LC_17b (both associated with decreased maximum velocity of shortening). DSM from dysfunctional bladder also exhibited tonic-type contractions, characterized by slow force generation and high force maintenance. Immunofluorescence microscopy showed that decreased SM-B expression in dysfunctional bladders was not due to generation of a new cell population lacking SM-B. Metabolic cage monitoring revealed decreased void volume and increased voiding frequency correlated with overexpression of SM-A and LC_17b. Myosin isoform expression and bladder function returned toward normal upon removal of the obstruction, indicating that the levels of expression of these isoforms are markers of the PBOO-induced dysfunctional bladders. bladder remodeling; bladder dysfunction; SM-A; LC_17a; benign prostatic hyperplasia     

Mir-29 Repression in Bladder Outlet Obstruction Contributes to Matrix Remodeling and Altered Stiffness

Recent work has uncovered a role of the microRNA (miRNA) miR-29 in remodeling of the extracellular matrix. Partial bladder outlet obstruction is a prevalent condition in older men with prostate enlargement that leads to matrix synthesis in the lower urinary tract and increases bladder stiffness. Here we tested the hypothesis that miR-29 is repressed in the bladder in outlet obstruction and that this has an impact on protein synthesis and matrix remodeling leading to increased bladder stiffness. c-Myc, NF-κB and SMAD3, all of which repress miR-29, were activated in the rat detrusor following partial bladder outlet obstruction but at different times. c-Myc and NF-κB activation occurred early after obstruction, and SMAD3 phosphorylation increased later, with a significant elevation at 6 weeks. c-Myc, NF-κB and SMAD3 activation, respectively, correlated with repression of miR-29b and miR-29c at 10 days of obstruction and with repression of miR-29c at 6 weeks. An mRNA microarray analysis showed that the reduction of miR-29 following outlet obstruction was associated with increased levels of miR-29 target mRNAs, including mRNAs for tropoelastin, the matricellular protein Sparc and collagen IV. Outlet obstruction increased protein levels of eight out of eight examined miR-29 targets, including tropoelastin and Sparc. Transfection of human bladder smooth muscle cells with antimiR-29c and miR-29c mimic caused reciprocal changes in target protein levels in vitro. Tamoxifen inducible and smooth muscle-specific deletion of Dicer in mice reduced miR-29 expression and increased tropoelastin and the thickness of the basal lamina surrounding smooth muscle cells in the bladder. It also increased detrusor stiffness independent of outlet obstruction. Taken together, our study supports a model where the combined repressive influences of c-Myc, NF-κB and SMAD3 reduce miR-29 in bladder outlet obstruction, and where the resulting drop in miR-29 contributes to matrix remodeling and altered passive mechanical properties of the detrusor.