兔膀胱出口部分梗阻所致逼尿肌超微结构的改变

目的　观察兔膀胱出口部分梗阻后逼尿肌细胞超微结构的改变。　方法　建立雄性兔膀胱出口部分梗阻动物模型 ,利用透射电镜观察其逼尿肌细胞内超微结构 ,应用ImagineTool图像分析软件检测粗面内质网面积和线粒体密度。　结果　梗阻组逼尿肌细胞内单位面积平均 1 1 5 .2 8μm2 ,胞质中粗面内质网面积 (5 .377± 2 .31 8) μm2 ,较对照组的 (0 .476± 0 .31 9) μm2 明显扩大 ;线粒体相对密度为 1 .0 2 7± 0 .0 64 ,较对照组的 0 .830± 0 .0 58明显下降 ,P均 <0 .0 1。　结论　膀胱出口部分梗阻后逼尿肌细胞内质网扩张 ,提示其合成蛋白质功能增强 ,从而引起膀胱壁增厚 ;而线粒体水肿明显 ,密度下降 ,提示逼尿肌细胞能量代谢障碍 ,导致其收缩功能下降     

膀胱出口部分梗阻对逼尿肌生物力学特性的影响

目的 探讨膀胱出口部分梗阻(P-BOO)对膀胱逼尿肌生物力学特性的影响及机制.方法 采用Wistar雄性大鼠,膀胱颈不全结扎法建立P-BOO动物模型.依据梗阻时间分为假手术组、梗阻6周组(P-B006W)及梗阻12周组(P-B0012W),其中P-B006W组根据充盈性膀胱测压所示逼尿肌是否稳定分为逼尿肌稳定组(DS)和逼尿肌不稳定组(DI).采用灌流肌槽,以拟胆碱药物(氯化氨基甲酰胆碱)作为刺激因素,用拉力传感器测定离体逼尿肌条的主动收缩功能.充盈性膀胱测压检测最大膀胱容量、膀胱漏尿点压及膀胱顺应性的变化.结果P-BOO模型均成功建立,DI组最大膀胱容量、膀胱漏尿点压、膀胱顺应性[(10.8±3.0)ml,(39.4±7.1)cm H20,(0.27±0.08)ml/cm H20]、DS组[(10.3±1.9)ml,(35.9±6.2)cm H2O,(0.29±0.05)ml/cm H2O]及P-B0012W组[(9.5±2.3)ml,(48.6±9.5)cm H20,(0.21±0.05)ml/cm H2O]均明显高于假手术组[(2.1±0.3)ml,(16.2±2.1)cm H2O,(0.13±0.03)ml/cm H2O],差异有统计学意义(P＜0.05).DI组逼尿肌条拟胆碱药物刺激产生的收缩力显著低于假手术组和DS组.P-B0012W组逼尿肌条均未检测到明确的收缩波(波幅＜0.05 g).结论 P-BOO后膀胱逼尿肌生物力学特性发生了改变:DI组逼尿肌收缩功能受损,DS组发生代偿,但如果梗阻未解除,则逼尿肌收缩性损害,最终导致不可逆的收缩功能丧失;梗阻后膀胱顺应性增大与膀胱容积显著增加密切相关,逼尿肌稳定性对其影响不显著.     

膀胱出口梗阻对逼尿肌功能的影响

膀胱出口梗阻 (BOO)常常导致逼尿肌功能改变 ,依膀胱出口梗阻的程度及时间的不同 ,逼尿肌功能变化有所差别 ,但BOO导致副尿肌功能变化的病理生理及最终结果却相对一致 ,包括逼尿肌不稳定 (DI)、逼尿肌收缩功能受损和逼尿肌顺应性改变。本文综合文献 ,对BOO后逼尿肌功能改变及其机制进行综述。     

tadenan对实验兔膀胱出口部分梗阻所致膀胱功能障碍的治疗作用

目的观察tadenan(太得恩,原名通尿灵)对膀胱出口部分梗阻所致膀胱功能障碍的治疗作用.方法20只新西兰雄性白兔分4组每组5只.A组为正常对照组,B、C、D组为实验组,A组行手术但不造成梗阻,B、C、D组手术造成膀胱出口部分梗阻.术后两周,B组予太得恩100mg*kg-1*d-1口服,C组予花生油(太得恩赋形剂),A、D组不给任何药物.饲养后解剖膀胱,取逼尿肌束标本于不同溶液中行电生理刺激观察其收缩功能,并以电子显微镜观察逼尿肌细胞超微结构.结果太得恩对膀胱出口部分梗阻所致的膀胱容量缩小有明显的保护作用;A组膀胱逼尿肌的收缩性明显优于D组及C组;D组和C组膀胱逼尿肌细胞中内质网明显扩张,线粒体水肿明显;而太得恩对逼尿肌细胞超微结构的病理改变具有保护作用.结论太得恩可保护膀胱逼尿肌收缩功能,对BPH有良好疗效.     

膀胱出口梗阻对逼尿肌功能的影响

膀胱出口梗阻（BOO）常常导致逼尿肌功能改变,依膀胱出口梗阻的程度及时间的不同,逼尿肌功能变化有所差别,但BOO导致逼尿肌功能变化的病理生理及最终结果却相对一致,包括逼尿肌不稳定（DI）,逼尿肌收缩功能受损和逼尿肌顺应性改变,本文综合文献,对BOO后逼尿肌功能改变及其机制进行综述。     

膀胱出口梗阻所致逼尿肌过度活动的神经电生理研究

目的 从膀胱传入神经以及盆底相关神经肌肉角度探讨神经因素及肌源性因素在膀胱出口梗阻所致的逼尿肌过度活动发生中的作用.方法 采用耻骨上膀胱颈梗阻的方法建立逼尿肌过度活动大鼠模型,测定不稳定收缩时盆神经传入电位信号,并同步测定阴部神经运动支电位、尿道外括约肌肌电及腹肌肌电的反射反应.并观察T8段脊髓截断、双侧盆神经截断、腹交感干截断以及双侧阴部神经截断后大鼠膀胱充盈测压不稳定收缩的变化.结果 成功制作了膀胱出口梗阻逼尿肌过度活动大鼠模型,成功率62.5%.充盈性膀胱测压神经肌电生理同步记录结果显示,允盈期逼尿肌过度活动可分为两种类型,一种为收缩幅度高于10 cmH2O(1 cmH2O=0.098 kPa)的逼尿肌过度活动(B-DO),伴有同步盆神经传入的信号明显增强,且能引发阴部神经、尿道外括约和腹肌肌电图出现显著变化;一种为收缩幅度低于10 cmH2O的逼尿肌过度活动(S-DO),没有上述盆神经传入及相关神经肌电变化.T8脊髓截断后,膀胱充盈-排尿收缩周期消失,膀胱基础压显著升高,B-DO消失,S-DO仍然存在,且收缩幅度较截断前略有上升,但差异无统计学意义.依次截断控制膀胱的盆神经、交感神经和阴部神经后,膀胱失去充盈-排尿收缩周期,基础压显著升高,不稳定收缩中B-DO消失,S-DO仍然存在.结论 膀胱出口梗阻所致的逼尿肌过度活动存在不依赖于中枢和周围神经的膀胱源性因素.     

前列腺增生症所致膀胱出口梗阻患者逼尿肌中神经生长因子mRNA的变化及意义

目的　探讨前列腺增生症 (BPH)所致膀胱出口梗阻 (BOO)患者膀胱逼尿肌中神经生长因子 (NGF)mRNA的表达变化及意义。方法　对同龄对照组 8例膀胱癌患者、BPH梗阻逼尿肌稳定组 2 4例患者和BPH梗阻逼尿肌不稳定组 16例患者的膀胱壁逼尿肌组织 ,采用逆转录聚合酶链反应(RT PCR)检测膀胱逼尿肌细胞中NGFmRNA的表达。结果　NGFmRNA在同龄对照组、BPH梗阻逼尿肌稳定组和梗阻逼尿肌不稳定组患者的膀胱逼尿肌细胞中均有表达 ,三组患者的平均表达水平两两之间差异均有显著性意义 (P <0 0 1) ,而且NGFmRNA在同龄对照组、BPH梗阻逼尿肌稳定组和梗阻逼尿肌不稳定组的平均表达水平逐渐增加。结论　前列腺增生症引起膀胱出口梗阻后 ,膀胱逼尿肌细胞中NGFmRNA表达水平增高 ,并可能与逼尿肌不稳定 (DI)的发生有关。     

前列腺增生症所致膀胱出口梗阻及其逼尿肌收缩力改变的定性和定…

经逼尿肌压与尿流率之间内关系的大量研究，创建了具有临床实用价值的诊断分析技术，在临床中具有重要的指导意义，本文详细介绍在压力－流率测定中几种临床实用的定性和定量诊断分析技术。     

膀胱出口梗阻时的逼尿肌不稳定（综述）

逼尿肌不稳定是造成尿频，尿急和急迫性尿失禁等症的主要原因之一，常继发于膀胱出口梗阻，在前列腺增生症中多见，与术后症状继续存在密切相关，近年，由于尿动力学技术的发展和应用，引起临床对此病的广泛关注。     

前列腺增生致膀胱出口梗阻患者逼尿肌神经生长因子表达及超微结构改变

目的通过人前列腺增生（BPH）致膀胱出口梗阻（BOO）后逼尿肌神经生长因子（NGF）表达及超微结构的研究揭示BOO后逼尿肌功能损害,了解BOO后膀胱逼尿肌的病理生理改变。方法免疫组化SABC法分实验组（梗阻组）33例和对照组（非梗阻组）15例,检测神经生长因子（NGF）的表达;超微结构实验组和对照组各5例,用电镜观察两组超微结构并对比。结果免疫组化梗阻组和非梗阻组NGF均表达,梗阻组表达明显高于非梗阻组（P〈0．01）;电镜部分对照组逼尿肌细胞排列整齐,细胞间隙有少量胶原纤维,细胞间以中间连接为主;实验组逼尿肌肥大,扭曲变形,排列不齐,增宽的细胞间隙中有大量的胶原纤维,细胞间中间连接减少,代替缝隙连接及桥粒连接等方式。结论BPH致BOO后膀胱逼尿肌细胞中NGF表达水平增高与逼尿肌不稳定（DI）及逼尿肌去神经改变等病理生理变化有关;BPH致BOO后逼尿肌不稳定及逼尿肌功能减退与逼尿肌形态改变及细胞连接等超微结构改变有关系。     

前列腺增生症的逼尿肌超微结构变化

为了研究前列腺增生症（ＢＰＨ）引起的膀胱逼尿肌超微结构变化，对１３例ＢＰＨ患者、９例同龄无膀胱颈梗阻（ＢＯＯ）老年人及８例正常青年人逼尿肌进行透射电镜观察。结果发现：ＢＰＨ的逼尿肌超微结构特点为：（１）平滑肌细胞（ＳＭＣ）肥大、扭曲变形，排列不齐；（２）ＳＭＣ之间的间隙明显增宽，内有大量胶原纤维，细胞间中间连接明显减少；（３）肌质膜内小泡小凹明显减少，细胞内肌丝萎缩，排列不齐，细胞器退变。认为ＢＰＨ超微结构变化的结果引起逼尿肌功能改变，从而加速ＢＰＨ的病理生理进程。     

经超声逼尿肌厚度测定在可疑膀胱出口梗阻患者中的应用

目的 分析可疑膀胱出口梗阻患者术前逼尿肌厚度,探讨逼尿肌厚度测定对可疑膀胱出口梗阻患者术后疗效的预测作用.方法 对可疑膀胱出口梗阻并行手术治疗的86例患者在行压力流率测定过程中,当膀胱容量为250 ml或灌注量为膀胱最大容量的50%时,应用7.5 MHz高频线纵超声探头行膀胱前壁逼尿肌厚度测定.术后3个月复查,将患者分为疗效显著组与疗效非显著组,比较2组患者年龄、前列腺体积及逼尿肌厚度.结果 疗效显著组(37例)与疗效非显著组(49例)患者年龄及前列腺体积差异无统计学意义(P＞0.05).逼尿肌厚度差异有统计学意义[(2.5±0.3)和(2.2±0.3)mm,P＜0.01].应用受试者工作特性曲线,当逼尿肌厚度≥2.8 mm时,逼尿肌厚度测定作为预测工作特异性和阳性预测值均为100%,而敏感性为19%,阴性预测值为62%.其曲线下面积为0.84±0.04.结论 逼尿肌测定预测可疑膀胱出口梗阻患者术后疗效可靠,但仍需要多中心、大样本的试验进一步确定临界值.

Abstract：

Objective To estimate the application of ultrasound measurement of detrusor wall thickness (DWT) in the assessment of curative effect after operation. Methods Detrusor thickness was measured by linear ultrasound (7. 5 MHz) either at a filling volume of 50% of cystometric capacity or at 250 ml filling in 86 patients, who were diagnosed equivocal BOO, during a pressure-flow study. All patients accepted transurethral resection of the prostate. At 3 months post-surgery, the patients were divided into two groups according to curative effect after operation. The volume of the prostate, age and DWT were compared between the two groups. Results There was no difference in either age or volume of the prostate between the two groups. DWT was significantly higher (P＜0.01) in the more curative effect group (37 cases, DWT 2. 5±0.3 mm) compared to the less curative effect group (49 cases, 2.2±0. 3 mm). As a predictor of curative effect, DWT of 2. 8 mm or greater had a positive predictive value of 100%, a negative predictive value of 62%, specificity of 100% and sensitivity of 19%. Receiver operating characteristic analysis (ROC) revealed that DWT had a high predictive value for curative effect post-surgery with an AUC of 0. 84±0. 04. Conclusions In patients with equivocal BOO, ultrasonographically assessed detrusor thickness may have a predictive value for curative effect post-surgery. However, this cutoff value needs to be validated in a larger study population.     

多沙唑嗪对兔膀胱出口部分梗阻致膀胱顺应性减低的影响

目的 探讨多沙唑嗪对兔膀胱出口部分梗阻后膀胱顺应性改变的影响.方法 成年雄性新西兰兔40只随机分为4组,每组10只,A组为假手术对照组,B组为膀胱出口部分梗阻组,C组为膀胱出口部分梗阻后口服多沙唑嗪组,D组为假手术后给予多沙唑嗪组.各组于14周行尿动力学检测,检测完成后处死并留取膀胱标本,行膀胱称重.结果 4组膀胱标本质量分别为(3.2±0.9)、(14.1±2.3)、(5.0±2.0)、(2.9±0.5)g;B、C组均高于A、D组,B组高于C组,差异均有统计学意义(P＜0.01);A、D组间比较差异无统计学意义(P＞0.05).4组逼尿肌漏尿点压分别为(10.2±2.5)、(18.8±6.1)、(13.5±4.7)、(11.6±3.6)cm H2O(1 cm H2O=0.098 kPa),B组高于A、D组,差异有统计学意义(P＜0.01),且高于C组,差异有统计学意义(P＜0.05);A、C、D组间差异无统计学意义(P＞0.05).膀胱顺应性分别为(2.86±0.56)、(1.22±0.39)、(4.25±2.19)、(2.90±0.53)ml/cm H2O,B组与A、D组相比明显下降,差异有统计学意义(P＜0.01);C组高于A、D组,差异有统计学意义(P＜0.05);A、D组间差异无统计学意义(P＞0.05).结论膀胱出口部分梗阻后早期应用多沙唑嗪治疗能够延迟梗阻对膀胱顺应性的损害,保护膀胱储尿功能.

Abstract：

Objective To explore the effect of doxazosin on rabbit bladder compliance after partial bladder outlet obstruction. Methods A total of 40 male New Zealand white rabbits were randomized into 4 groups, with 10 rabbits in each group. Partial bladder outlet obstruction was established in groups B and C, while groups A and D underwent the same operation but without partial bladder outlet obstruction. On the day after the operation, groups C and D received oral administration of doxazosin. After 14 weeks, urodynamic examinations were carried out in all groups, and the bladder was weighted after cystectomy. Results Bladder weight was (3.2±0.9) g in group A, (14.1±2.3) g in group B, (5.0±2.0) in group C,and (2.9±0.5) g in group D. The bladder weight in groups B and C increased significantly compared to groups A and D (P＜0.01), group B increased significantly over group C (P＜0.01), and there was no significant difference between groups A and D (P＞0.05).The detrusor leak point pressure was (10.2±2.5) cm H2O in group A, (18.8±6.1) cm H2O in group B, (13.5±4.7) cm H2O in group C,and (11.6±3.6) cm H2O in group D. The detrusor leak point pressure in group B was significantly higher than group A, group D (P＜0.01) and group C (P＜0.05). There was no significant difference between group A, group C and group D (P＞0.05). The bladder compliance was (2.86±0.56) ml/cm H2O in group A, (1.22±0.39) ml/cm H2O in group B, (4.25±2.19) ml/cm H2O in group C,and (2.90±0.53) ml/cm H2O in group D. The bladder compliance was significantly decreased in group B compared to groups A and D (P＜0.01). Bladder compliance in group C was significantly higher than in groups A and D (P＜0.05), and there was no significant difference between group A and group D (P＞0.05). Conclusion Early use of doxazosin can delay the occurrence of lower bladder compliance after partial bladder outlet obstruction, thus protecting the storage function of bladder.     

人膀胱出口梗阻后逼尿肌酶学和形态学异常的研究

目的探讨人膀胱出口梗阻(BOO)后逼尿肌酶学和形态学的变化及意义。方法采集8例无BOO膀胱肿瘤患者及8例伴BOO良性前列腺增生患者的膀胱逼尿肌肌条,分别对组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)、Ca2+Mg2+-ATP酶活性进行测定,并做电镜观察。结果对照组膀胱逼尿肌组织中SOD活性(20.39±2.02)U/mg蛋白、NOS活性(1.81±0.38)U/mg蛋白,Ca2+Mg2+-ATP酶活性(1.47±0.43)μmol P i/mg蛋白,BOO组则分别为(12.77±2.62)U/mg蛋白,(1.36±0.22)U/mg蛋白,(0.97±0.33)μmol P i/mg蛋白(P<0.05),BOO组MDA含量(1.70±0.22)nmol/mg蛋白低于BOO组(2.42±0.69)nmol/mg蛋白(P<0.05)。电镜观察BOO组逼尿肌细胞中粗面内质网明显扩张、脱颗粒,线粒体水肿明显、空泡变性和线粒体内嵴减少、消失,有的细胞内可见大量溶酶体。结论人BOO后缺血再灌注参与人逼尿肌功能失代偿的演化过程,减少自由基产生和避免过度超氧化反应仍是防止或减缓BOO后膀胱逼尿肌发生一系列病理变化的关键。     

The detrusor muscle: an innocent victim of bladder outlet obstruction

OBJECTIVES: Benign prostatic hyperplasia (BPH) is considered a frequent cause of bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTS), although the physiopathologic mechanism through which BPH causes LUTS is not clear. Several morphologic and functional modifications of the bladder detrusor have been described in patients with BPH and could play a direct role in determining symptoms. The opinion is spreading that the enlarged prostates in patients with LUTS is nothing more than a mere bystander. Evidence has accumulated, however, supporting the role of BPH-related BOO as the direct cause determining bladder dysfunction and indirectly causing urinary symptoms. The present review addresses the bladder response to BOO, particularly focusing on the physiopathologic cascade that links obstructive BPH to bladder dysfunction. METHODS: A literature review of peer-reviewed articles has been performed, including both in vivo and in vitro studies on human tissue and animal model experiments. RESULTS: Epithelial and smooth muscle cells in the bladder wall are mechanosensitive, and in response to mechanical stretch stress caused by BOO, undergo modifications of gene expression and protein synthesis. This process involves several transduction mechanisms and finally alter the ultrastructure and physiology of cell membranes, cytoskeleton, contractile proteins, mitochondria, extracellular matrix, and neuronal networks. CONCLUSIONS: BOO is the initiator of a physiopathologic cascade leading to deep changing of bladder structure and function. Before being a direct cause of storing-phase urinary symptoms, the bladder is the first innocent victim of prostatic obstruction.     

逼尿肌自身肌源性变化与逼尿肌不稳定的关系

目的:探讨逼尿肌不稳定(Detrusor instability,DI)的发病机制。方法:建立Wistar大鼠膀胱流出道梗阻(Bladder outlet obstruction,BOO)动物模型,6周后行充盈性膀胱测压分出梗阻后稳定组和不稳定组,进行离体膀胱充盈性测压、逼尿肌条机械牵拉及胆碱类药物刺激试验。结果:不稳定组膀胱充盈至出现收缩时的压力明显低于稳定组及正常对照组,收缩发生时的容积明显低于稳定组;不稳定组逼尿肌条机械牵拉至其出现收缩时的最小张力明显低于稳定组及正常对照组;不同浓度氯化氨基甲酰胆碱刺激诱发的收缩频率各组间差异无统计学意义(P<0.05)。结论:逼尿肌不稳定的发生与逼尿肌自身的兴奋性增强密切相关。     

The rate of urgency symptoms in women with stress urinary incontinence and nomogram based bladder outlet obstruction

We reviewed the charts of 132 women 30 of whom were chosen asobstructed, 30 equivocal and 72 as unobstructed by automatically givennomograms in the urodynamic evaluation for stress incontinence. Therates of urgency symptoms in nomogram based obstructed, equivocal andunobstructed cases of stress incontinence were found in 30%,23.3% and 12.5% respectively. More urgency symptoms wereobserved in women with stress incontinence and nomogram based bladderoutlet obstruction than in equivocal and unobstructed cases. This revised version was published online in August 2006 with corrections to the Cover Date.     

膀胱出口梗阻指数在评估良性前列腺增生症膀胱出口梗阻中的应用

目的 探讨膀胱出口梗阻指数(BOON)在评估前列腺增生患者膀胱出口梗阻(BOO)中的意义.方法 对临床有下尿路症状,怀疑存在因前列腺增生症(BPH)导致膀胱出口梗阻的76例患者,测定前列腺体积(经直肠),最大自由尿流率(Qmax)和平均排尿量,通过公式计算BOON=前列腺体积(cm3)-3×Qmax(ml/s)-0.2×平均排尿量(ml).同时对患者进行压力.流率测定,计算AG值和Schafer梗阻级别,与BOON对照,分析利用BOON评估膀胱出口梗阻的准确性.结果 将本组患者年龄、前列腺体积、最大尿流率、残余尿量及BOON值,以AG作为因变量,同AG进行多元线性回归分析.整体回归方程中R=0.542(P=0.000),其中BOON值同AG值相关性最强(P=0.000).18例BOON值>-10,此时利用BOON判断BOO的敏感性为31%,特异性为100%,取BOON>-20时,敏感性为42.4%,特异性为88.2%;取BOON>-30时,敏感性为66.1%,特异性为82.4%;而取BOON>-40时,敏感性为77.9%,其特异性为64.7%.取BOON值-30作为分界点,在不明显降低特异性的同时,能够更敏感的判断BOO,BOON数值越大,利用BOON判断膀胱出口梗阻的特异性越高.结论 通过测定前列腺体积,最大自由尿流率(Qmax)和平均排尿量计算膀胱出口梗阻指数,取BOON>-30为分界点,是预测前列腺增生症是否存在膀胱出口梗阻的一种简易、无创方法,具有较好的特异性和敏感性.