前列腺增生症患者剩余尿与膀胱出口梗阻逼尿肌收缩力的相关性研究

目的 :探讨前列腺增生症 (BPH)患者剩余尿 (RUV )与膀胱出口梗阻 (BOO)、逼尿肌收缩力相关性。方法 :对 42例 BPH患者进行尿动力学检查。结果 :RUV与 BOO呈正相关 (r =0 .716 0 ,P <0 .0 1) ,与逼尿肌等容收缩压 (Piso)呈负相关 (r =- 0 .5 718,P <0 .0 1)。术前和术后的 RU V、尿道阻力因子 (URA )的差异有显著性意义 (P<0 .0 5 ) ,而术前和术后的 Piso差异无显著性意义 (P>0 .0 5 )。结论 :BPH患者 RUV的产生及增多是由于 BOO的加重和逼尿肌功能受损的共同结果 ,在病程的不同阶段 ,BOO和逼尿肌收缩力对 RUV的产生、增多及减少具有不同的作用和意义。     

膀胱出口梗阻对逼尿肌兴奋性、收缩性及顺应性影响的实验研究

目的 探讨膀胱出口梗阻（ＢＯＯ）对逼尿肌兴奋性、收缩性、顺应性的影响及逼尿肌不稳定（ＤＩ）的发病机理。方法 建立Ｗｉｓｔａｒ大鼠ＢＯＯ动物模型,６周后行充盈性膀胱测压及离体逼尿肌条机械牵拉、电及胆碱类药物刺激试验。结果 ＢＯＯ后ＤＩ的发生率为６９％,逼尿肌顺应性升高;ＤＩ组与梗阻后稳定组及正常对照组相比,牵引逼尿肌致其出现心地的张力明显了低,电刺激产生的收缩力明显减弱;ＤＩ组逼尿肌胆碱类药物刺激产     

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。     

良性前列腺增生患者膀胱出口梗阻和逼尿肌功能的分析

目的：探讨尿动力学检查对BPH患者膀胱出口梗阻（BOO）和逼尿肌功能的诊断意义.方法：对95例BPH患者进行压力-容积和压力-流率测定.结果：95例BPH患者中BOO 57例,无BOO23例,其余15例为可疑或分析困难.BOO组前列腺体积大于无BOO组（62.4±16.1）cm^3 vs（41.0±7.1）cm^3（P＜0.05）,最大尿流率（Qmax）小于无BOO组（5.4±1.9）ml/s vs（12.4±5.0）ml/s（P＜0.05）,两组IPSS评分无差别（23.7±4.4）分vs（25.2±4.9）分（P＞0.05）.BOO组有逼尿肌不稳定收缩（DD34例,无BOO组D119例.结论：尿动力学检查有助于判断有无BOO存在,了解BPH患者的逼尿肌功能.IPSS不能判断患者的下尿路症状（LUTS）是否因BOO导致.BPH患者前列腺体积不足很大,但LUTS明显时,应行尿动力学检查.自由尿流率测定对BOO诊断有一定帮助.DI是无BOO患者发生LUTS的重要因素.     

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状的主要原因之一,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,引起临床对此症的广泛关注。     

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量分析(文献综述)

经逼尿肌压与尿流率之间内在关系的大量研究，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。     

膀胱出口部分梗阻（PBOO）引起逼尿肌肥大、收缩力降低及逼尿肌收缩和调控蛋白的改变

膀胱出口部分梗阻(PBOO)引起导致排尿次数增加、每次尿量减少、逼尿肌肥大以及逼尿肌收缩和调控蛋白的改变。作者希望明确PBOO诱导的尿频及逼尿肌肥大,是否与尿道平滑肌收缩能力及肌球蛋白亚型的表达相关。通过外科手术构建标准新西兰白兔PBOO模型,以假手术组作为对照。手术后12d,通过代谢笼监测24h的排尿次数及每次尿量。每24h排尿(43±12)次(梗阻组)、(6±3)次(假手术组)的兔子进入研究。通过光镜及免疫荧光显微镜检查尿道的形态学改变。肌球蛋白亚型在mRNA及蛋白水平的表达通过RT-PCR及Western blotting检测。结果发现PBOO白兔…     

良性前列腺增生患者残余尿量与膀胱出口梗阻和逼尿肌收缩力的相关性研究

目的:探讨良性前列腺增生(BPH)患者残余尿量(VRU)与膀胱出口梗阻(BOO)程度和逼尿肌收缩力的相关性。方法:临床诊断为BPH的患者152例,均行B超检查测量前列腺体积(PV)和膀胱VRU,自由尿流率检测,全套尿动力学检查评估BOO程度和逼尿肌收缩力。采用SPSS 20.0统计软件,对B超和尿动力学参数行相关性分析,两样本均数比较采用t检验,定义P0.05有统计学意义。结果:PV与BOO程度和逼尿肌收缩力有正相关性(相关系数r=0.432和r=0.343,P0.01)。最大尿流率(Qmax)与BOO程度负相关(r=-0.327,P0.01),而与逼尿肌收缩力无显著相关性(r=0.123,P0.05)。VRU≤150 ml时,VRU与逼尿肌收缩力间无显著相关性(r=0.041,P0.05);当VRU150 ml时,VRU与逼尿肌收缩力有显著负相关性(r=-0.490,P0.01);VRU300 ml时,该相关性尤为明显(r=-0.717,P0.01)。结论:VRU对逼尿肌功能有一定预测价值。VRU150 ml者应重视逼尿肌功能的评估,尤其是VRU300 ml时,建议行尿动力学检查以正确评估BOO程度和逼尿肌收缩力。     

The routine assessment of detrusor contraction strength

A method is described for the semiquantitative assessment of the strength of the detrusor contraction during any voiding for which the detrusor pressure, flow rate, and residual urine are measured. A computer is used to produce plots of detrusor pressure vs detrusor shortening velocity throughout voiding. The adequacy of the contraction can be followed through micturition until the bladder is nearly empty. In some cases the isovolumetric detrusor pressure and the maximum potential velocity of shortening of the detrusor can be estimated. The ranges of values found are comparable with those deduced from the stop test, although there are slight discrepancies. The median values of these two parameters form the basis of the routine method that can be used for any detrusor contraction.     

毒蕈碱受体亚型介导逼尿肌细胞收缩与IP3关系的实验研究

目的　探讨信使分子IP3 在毒蕈碱受体亚型M3 R介导逼尿肌细胞收缩中的作用。　方法　MR非选择性激动剂 (carbachol)、拮抗剂 (atropine)及M2 R拮抗剂 (methoctramine)、M3 R拮抗剂 (4 DAMP)刺激原代培养人逼尿肌细胞 ,通过 [3 H]掺入法 ,检测磷脂酰肌醇 (PI)代谢产物 [3 H] IP含量。　结果　 [3 H] IP含量随carbachol刺激浓度增加而增加 ;10 -9、10 -8、10 -7、10 -6、10 -5、10 -4mmol/L的 4 DAMP抑制carbachol后 ,[3 H] IP含量分别为 392 6 .5 7± 2 73.2 9、2 780 .5 2± 2 11.0 9、2 4 36 .84± 15 3.6 2、1973.2 2± 16 4 .71、1372 .38± 14 1.35及 110 7.98± 92 0 .4 5cpm ,相同浓度的at ropine作用后 ,[3 H] IP含量分别为 36 0 2 .6 9± 2 80 .17、2 891.31± 2 0 7.4 5、1983.97± 14 5 .74、12 6 9.5 7± 10 5 .31、110 6 .37± 75 .2 3、92 7.5 0± 77.36cpm ;而相同浓度的methoctramine作用后 ,[3 H] IP含量分别为 4 4 6 2 .74± 36 0 .6 9、3938.6 1± 32 7.13、3315 .4 5± 2 70 .36、30 6 3.19± 2 4 6 .79、2 92 7.37± 2 2 6 .4 5及 2 836 .5 5± 2 4 1.6 3cpm ,两者之间差异有非常显著性意义 (P <0 .0 1) ,表明 4 DAMP和atropine能显著抑制carbachol诱导的代谢反应 ,而methoctram     

Prazosin treatment of neurological patients with detrusor hyperreflexia and bladder emptying disability

In a placebo-controlled clinical trial with cross-over design the effect of alpha-adrenoceptor blockade with prazosin was studied in 18 neurological patients with detrusor hyperreflexia and bladder emptying disability. During active treatment both the distance to maximal urethral closure pressure (MUCP) and MUCP were significantly reduced. In addition, the volume at first bladder contraction was increased. The urodynamic parameters measured during voiding were unaffected. We conclude that prazosin decreases detrusor hyperreflexia but only in rare cases may benefit bladder emptying in these patients.     

糖尿病膀胱顺应性及逼尿肌舒缩功能的实验研究

目的　为进一步阐明糖尿病膀胱病变的发病机理提供实验依据。　方法　以糖尿病大鼠为模型 ,蔗糖利尿鼠及正常大鼠为对照 ,作离体膀胱灌注测压观察膀胱顺应性改变 ;分别采用全膀胱及逼尿肌条对比研究膀胱舒缩功能变化。　结果　糖尿病组大鼠膀胱逼尿肌收缩力明显低于蔗糖利尿组及对照组 [分别为 (2 0 80± 6 38)、(31 6 6± 6 17)、(4 0 10± 7 2 1)g/ 10 0mgT];膀胱舒张功能显著下降 ,膀胱顺应性升高。　结论　糖尿病大鼠模型 12周时膀胱收缩、舒张功能明显受损 ,同时 ,膀胱顺应性异常也是致病机理之一 ;利尿 (多尿 )不是糖尿病膀胱病变的主要因素。     

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。     

Cooling-induced bladder contraction: studies on isolated detrusor muscle preparations in the rat

OBJECTIVES: Detrusor muscle contraction and uninhibited micturition after intravesical instillation of ice water is interpreted as a sign of upper motor neuron lesions. The basic mechanism of cooling-induced contraction (CIC) at the level of smooth muscle, however, has not been satisfactorily explained. We therefore designed model experiments with cooling of rat detrusor muscle. METHODS: We recorded isometric tension from strips of rat urinary detrusor muscle in organ baths during stepwise cooling. CIC was tested before and after addition of various standard agents interfering with known neurogenic (autonomic blockers, tetrodotoxin, capsaicin) and myogenic mechanisms of contraction (calcium channel blockers). RESULTS: Stepwise cooling (37 degrees to 5 degrees C) of detrusor muscle induced reproducible graded contractions, inversely proportional to temperature. CIC was not dependent on a neural mechanism (not blocked by tetrodotoxin or capsaicin) or the release of neurotransmitters but was linked to translocation of calcium. It was reduced by calcium channel blockers and Ca(2+)-free solution. Blockage of the Ca(2+)-adenosine triphosphatase pump, which inhibits the extrusion of calcium, also plays a significant role in the process and enhances CIC. CONCLUSIONS: Cooling of detrusor muscle preparations induces a graded myogenic contraction inversely proportional to the temperature. The mechanism is not dependent on local nervous control but is related to calcium translocation.     

Urgency degree and bladder contraction velocity: sequential changes in women with idiopathic detrusor overactivity

AIMS: In patients with idiopathic detrusor overactivity (DO) who showed storage symptoms worsening with time, we checked whether and which urodynamic parameter changes are associated with an increased urgency degree. MATERIALS AND METHODS: We analyzed retrospectively the urodynamic findings in 54 women -27 with storage symptoms (Group A, mean age 32 +/- 7 years) and 27 controls (Group B, mean age 30 +/- 9 years). These latter had a history of recurrent UTIs (urinary tract infections), but when seen by us had no UTI, DO, lower urinary tract symptoms, or any other pathological finding. Group A had a first urodynamic examination when first referred (time 1) and were re-assessed a mean of 16 months later (time 2) for worsened storage symptoms. RESULTS: In Group A, an idiopathic DO was shown at both times 1 and 2; urgency of voiding could be delayed during cystometry for >or=2 min (= moderate urgency) at time 1 and for <2 min (= severe urgency) at time 2; detrusor contraction strength or contractility proved higher than in Group B (P < 0.001) and increased from time 1 to time 2 (P < 0.001), detrusor shortening velocity being always the major component of the higher contractility levels. CONCLUSIONS: A DO-related increase in bladder contractility may have been further enhanced by severe urgency through a positive feedback mechanism. The urgency degree proved closely associated in DO patients with the level of detrusor shortening velocity rather than with detrusor pressure.     

前列腺增生患者逼尿肌收缩曲线下面积相关参数与膀胱出口梗阻的关系

目的 分析逼尿肌收缩曲线下面积相关参数与BOO的关系,探讨逼尿肌收缩曲线下面积相关参数用于诊断BOO的可行性. 方法 2006年10月至2008年10月对138例BPH患者行尿动力学检查,通过AG数和直线被动尿道阻力关系(Lin-PURR)将患者分为无梗阻、可疑梗阻和梗阻3组.计算排尿时逼尿肌收缩曲线下面积(AUCdet)、排尿时逼尿肌收缩曲线下面积与排尿量的比值(AUCdet/Vol),并与AG数和Lin-PURR做相关性检验,使用线性区别分析方法 对AUCdet/Vol 关于无梗阻、可疑梗阻和梗阻的分类与传统方法 进行比较. 结果 AUCdet、AUCdet/Vol与AG数、Lin-PURR具有很好的相关性(均P＜0.001).109例患者根据AG数和Lin-PURR进入下一步分析,其中无梗阻33例、可疑梗阻32例、梗阻44例.3组患者AUCdet分别为(766±354)、(1214±800)、(2294±1166)cm H2O·s,AUCdet/Vol分别为(5.47±2.26)、(9.65±4.94)、(20.03±10.86)crn H2O·s/ml,组间比较差异均有统计学意义(均P＜0.001).AUCdet/Vol诊断BOO与传统分组方法 的总符合率为68.8%(75/109),其中诊断无梗阻、可疑梗阻和梗阻的符合率分别为90.9%(30/33)、43.8%(14/32)和70.5%(31/44). 结论 应用逼尿肌收缩曲线下面积相关参数可以很好地反映BOO情况.     

NGF与神经源性膀胱逼尿肌功能研究进展

随着NGF及其受体研究的深入,学者们发现NGF与膀胱功能有着密不可分的关系,NGF在膀胱疾病中的作用也越来越受到重视,研究发现膀胱组织能够在一些特定情况下增加NGF的表达,例如脊髓损伤、去神经化、炎症、膀胱过度活动等.NGF水平的变化会导致多种临床症状,如排尿功能紊乱、膀胱过度活动的产生及进展、膀胱疼痛(间质性膀胱炎)...     

Relationship between gastric emptying of liquid and postvagotomy diarrhoea

Gastric emptying of liquid was studied in 10 normal volunteers and in 27 patients previously treated with truncal vagotomy and drainage. Thirteen of the twenty-seven patients complained of persistent postvagotomy diarrhoea. For each study 300 ml 15 per cent dextrose, labelled with 99mTc-diethylene triamine penta-acetic acid (DTPA), was ingested at a standard rate by subjects who sat facing a gamma camera. Imaging proceeded for 30 min. Gastric area activity curves were corrected for emptying of the test meal during ingestion, and for movement using a new image alignment technique. Gastric emptying at 15 min was 10 +/- 2.6 per cent (mean +/- s.e.m.) in healthy volunteers, 48 +/- 7.3 per cent in patients without diarrhoea, and 84 +/- 2.3 per cent in those with diarrhoea (P less than 0.001, ANOVA). Gastric emptying from 15 min onwards was slower than normal in both patient groups (P less than 0.001). These results show that initial gastric emptying is rapid following truncal vagotomy and drainage, and this change is greater in patients with postvagotomy diarrhoea. No patient with diarrhoea had normal initial gastric emptying.