Dataset Information

Urodynamic characteristics of detrusor underactivity in women with voiding dysfunction.

ABSTRACT:

Introduction and hypothesis

Voiding dysfunction has gained interest due to its high prevalence in the elderly. This study characterized bladder dysfunction in women with voiding dysfunction using video urodynamic studies (VUDS) focused on detrusor underactivity (DU).

Methods

We studied 1914 women in which first-line medical treatment failed. Age, comorbidities, and urodynamic parameters were analyzed to determine the association between bladder sensation and contractility.

Results

VUDS were normal in 2.9% (n = 56) of patients and showed DU in 23.1% (n = 443), detrusor hyperactivity and impaired contractility (DHIC) in 12.0% (n = 231), hypersensitive bladder in 17.0% (n = 325), detrusor overactivity (DO) in 2.6% (n = 49) and bladder outlet obstruction in 42.3% (n = 810). The mean age of patients in the DU and DHIC groups was significantly older than in women with normal VUDS and those with hypersensitive bladders (p<0.01). Decreased bladder sensation and larger cystometric bladder capacity were noted in the DU group compared to the DHIC, HSB, and DO groups. Bladder sensation was negatively associated with the bladder contractility. Bladder contractility index and voiding efficiency were lower in the DU and DHIC groups compared to the normal group.

Conclusions

The bladder conditions of women with voiding dysfunction included DU, DHIC, HSB and DO. Bladder contractility index and voiding efficiency were significantly lowest in DU and DHIC groups and lower in HSB and DO groups than normal tracing group. Reduced bladder sensation was noted in DU and negatively associated with detrusor contractility.

SUBMITTER: Yang TH

PROVIDER: S-EPMC6010249 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Publications

Urodynamic characteristics of detrusor underactivity in women with voiding dysfunction.

Yang Tsai-Hwa TH Chuang Fei-Chi FC Kuo Hann-Chorng HC

PloS one 20180620 6

<h4>Introduction and hypothesis</h4>Voiding dysfunction has gained interest due to its high prevalence in the elderly. This study characterized bladder dysfunction in women with voiding dysfunction using video urodynamic studies (VUDS) focused on detrusor underactivity (DU).<h4>Methods</h4>We studied 1914 women in which first-line medical treatment failed. Age, comorbidities, and urodynamic parameters were analyzed to determine the association between bladder sensation and contractility.<h4>Resu ...[more]

PMID: 29924821

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Project description:BackgroundPreviously published results from our laboratory identified a mechano-gated two-pore domain potassium channel, TREK-1, as a main mechanosensor in the smooth muscle of the human urinary bladder. One of the limitations of in vitro experiments on isolated human detrusor included inability to evaluate in vivo effects of TREK-1 on voiding function, as the channel is also expressed in the nervous system, and may modulate micturition via neural pathways. Therefore, in the present study, we aimed to assess the role of TREK-1 channel in bladder function and voiding patterns in vivo by using TREK-1 knockout (KO) mice.MethodsAdult C57BL/6 J wild-type (WT, N = 32) and TREK-1 KO (N = 33) mice were used in this study. The overall phenotype and bladder function were evaluated by gene and protein expression of TREK-1 channel, in vitro contractile experiments using detrusor strips in response to stretch and pharmacological stimuli, and cystometry in unanesthetized animals.ResultsTREK-1 KO animals had an elevated basal muscle tone and enhanced spontaneous activity in the detrusor without detectable changes in bladder morphology/histology. Stretch applied to isolated detrusor strips increased the amplitude of spontaneous contractions by 109% in the TREK-1 KO group in contrast to a 61% increase in WT mice (p ≤ 0.05 to respective baseline for each group). The detrusor strips from TREK-1 KO mice also generated more contractile force in response to electric field stimulation and high potassium concentration in comparison to WT group (p ≤ 0.05 for both tests). However, cystometric recordings from TREK-1 KO mice revealed a significant increase in the duration of the intermicturition interval, enhanced bladder capacity and increased number of non-voiding contractions in comparison to WT mice.ConclusionsOur results provide evidence that global down-regulation of TREK-1 channels has dual effects on detrusor contractility and micturition patterns in vivo. The observed differences are likely due to expression of TREK-1 channel not only in detrusor myocytes but also in afferent and efferent neural pathways involved in regulation of micturition which may underly the "mixed" voiding phenotype in TREK-1 KO mice.

Project description:Mesenchymal stem/stromal cell (MSC) therapy is a promising approach for treatment of as yet incurable detrusor underactivity (DUA), which is characterized by decreased detrusor contraction strength and/or duration, leading to prolonged bladder emptying. In the present study, we demonstrated the therapeutic potential of human embryonic stem cell (ESC)-derived multipotent MSCs (M-MSCs) in a diabetic rat model of DUA. Diabetes mellitus (DM) was induced by intraperitoneal injection of streptozotocin (STZ) (50 mg/kg) into 8-week-old female Sprague-Dawley rats. Three weeks later, various doses of M-MSCs (0.25, 0.5, and 1 × 106 cells) or an equivalent volume of PBS were injected into the outer layer of the bladder. Awake cystometry, organ bath, histological, and gene expression analyses were evaluated 1 week (short-term) or 2 and 4 weeks (long-term) after M-MSC transplantation. STZ-induced diabetic rats developed DUA, including phenotypes with significantly longer micturition intervals, increased residual urine amounts and bladder capacity, decreased micturition pressure on awake cystometry, and contractile responses to various stimuli in organ bath studies. Muscle degeneration, mast cell infiltration, fibrosis, and apoptosis were present in the bladders of DM animals. A single local transplantation of M-MSCs ameliorated DUA bladder pathology, including functional changes and histological evaluation, and caused few adverse outcomes. Immunostaining and gene expression analysis revealed that the transplanted M-MSCs supported myogenic restoration primarily by engrafting into bladder tissue via pericytes, and subsequently exerting paracrine effects to prevent apoptotic cell death in bladder tissue. The therapeutic efficacy of M-MSCs was superior to that of human umbilical cord-derived MSCs at the early time point (1 week). However, the difference in efficacy between M-MSCs and human umbilical cord-derived MSCs was statistically insignificant at the later time points (2 and 4 weeks). Collectively, the present study provides the first evidence for improved therapeutic efficacy of a human ESC derivative in a preclinical model of DM-associated DUA.

Project description:BackgroundThe therapeutic effects of human embryonic stem cell-derived multipotent mesenchymal stem cells (M-MSCs) were evaluated for detrusor underactivity (DUA) in a rat model with atherosclerosis-induced chronic bladder ischemia (CBI) and associated mechanisms.MethodsSixteen-week-old male Sprague-Dawley rats were divided into five groups (n = 10). The DUA groups underwent 30 bilateral repetitions of endothelial injury to the iliac arteries to induce CBI, while the sham control group underwent a sham operation. All rats used in this study received a 1.25% cholesterol diet for 8 weeks. M-MSCs at a density of 2.5, 5.0, or 10.0 × 105 cells (250 K, 500 K, or 1000 K; K = a thousand) were injected directly into the bladder 7 weeks post-injury, while the sham and DUA group were treated only with vehicle (phosphate buffer solution). One week after M-MSC injection, awake cystometry was performed on the rats. Then, the bladders were harvested, studied in an organ bath, and prepared for histological and gene expression analyses.ResultsCBI by iliac artery injury reproduced voiding defects characteristic of DUA with decreased micturition pressure, increased micturition interval, and a larger residual volume. The pathological DUA properties were improved by M-MSC treatment in a dose-dependent manner, with the 1000 K group producing the best efficacy. Histological analysis revealed that M-MSC therapy reduced CBI-induced injuries including bladder fibrosis, muscular loss, and apoptosis. Transplanted M-MSCs mainly engrafted as vimentin and NG2 positive pericytes rather than myocytes, leading to increased angiogenesis in the CBI bladder. Transcriptomes of the CBI-injured bladders were characterized by the complement system, inflammatory, and ion transport-related pathways, which were restored by M-MSC therapy.ConclusionsSingle injection of M-MSCs directly into the bladder of a CBI-induced DUA rat model improved voiding profiles and repaired the bladder muscle atrophy in a dose-dependent manner.

Dataset Information

Urodynamic characteristics of detrusor underactivity in women with voiding dysfunction.

Introduction and hypothesis

Methods

Results

Conclusions

Publications

Urodynamic characteristics of detrusor underactivity in women with voiding dysfunction.

Similar Datasets

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