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      Do functional changes occur in the bladder due to bladder outlet obstruction? ‐ ICI‐RS 2018

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          Abstract

          Studies on bladder dysfunction (BD), more specifically functional‐urodynamic changes in the bladder as a result of bladder outlet obstruction (BOO) have been summarized for this TT. Based on available, but limited evidence from human studies a three‐stage model can be hypothesized to characterize BOO‐induced bladder remodeling: hypertrophy, compensation (increased detrusor contractility during the voiding phase, often in combination with filling phase detrusor overactivity) followed by the phase of decompensation [detrusor underactivity]. The time between the start of compensation and eventual decompensation seems to be determined by age of onset, severity, and type of obstruction and clinical mitigating factors such as vascular and metabolic problems. Understanding the relative contributions of these factors may allow the development of personalized timelines and probabilities for these obstructed patients.

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          Most cited references40

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          Progressive bladder remodeling due to bladder outlet obstruction: a systematic review of morphological and molecular evidences in humans

          Background Bladder outlet obstruction is a common urological condition. We aimed to summarize available evidences about bladder outlet obstruction-induced molecular and morphological alterations occurring in human bladder. Methods We performed a literature search up to December 2017 including clinical and preclinical basic research studies on humans. The following search terms were combined: angiogenesis, apoptosis, bladder outlet obstruction, collagen, electron microscopy, extracellular matrix, fibrosis, hypoxia, histology, inflammation, innervation, ischemia, pressure, proliferation, remodeling, suburothelium, smooth muscle cells, stretch, urothelium. Results We identified 36 relevant studies. A three-stages model of bladder wall remodeling can be hypothesized involving an initial hypertrophy phase, a subsequent compensation phase and a later decompensation. Histological and molecular alterations occur in the following compartments: urothelium, suburothelium, detrusor smooth muscle cells, detrusor extracellular matrix, nerves. Cyclic stretch, increased hydrostatic and cyclic hydrodynamic pressure and hypoxia are stimuli capable of modulating multiple signaling pathways involved in this remodeling process. Conclusions Bladder outlet obstruction leads to progressive bladder tissue remodeling in humans. Multiple signaling pathways are involved.
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            The effect of atherosclerosis-induced chronic bladder ischemia on bladder function in the rat.

            To develop a rat model of atherosclerosis-induced chronic bladder ischemia and investigate the effect of chronic bladder ischemia on voiding behavior and bladder function. Adult male rats were divided into three groups. The arterial injury (AI) group underwent endothelial injury of the iliac arteries and received a 2% cholesterol diet. The sham group underwent sham operation and received a 2% cholesterol diet. The control group received a regular diet. After 8 weeks, a metabolic cage study and cystometry were performed without anesthesia. Bladder blood flow was measured using a laser Doppler blood flowmeter. Histological examination of the iliac arteries and the bladder was performed. The bladder was also processed for immunohistochemical staining of oxidative stress markers. The metabolic cage study showed that in the AI group, voiding frequency significantly increased while voided volume significantly decreased. Cystometry showed that the frequency of reflex bladder contractions was significantly higher in the AI group. Filling-induced decrease in bladder blood flow was the greatest in the AI group. Histological study showed that in the AI group alone, atherosclerotic occlusion occurred in the iliac arteries as well as in the downstream bladder microvessels. Oxidative stress marker positive cells were more prevalent in the AI bladder than in the other bladders. Combined with a high-cholesterol diet, endothelial injury of iliac arteries induced arterial occlusive disease in the downstream vessels and consequent bladder ischemia in rats. This model of chronic bladder ischemia showed detrusor overactivity manifested as an increase in voiding frequency. Copyright © 2011 Wiley Periodicals, Inc.
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              Bladder outlet obstruction: progression from inflammation to fibrosis.

              To investigate the progression of urodynamic changes, as well as histological and biochemical outcomes over a prolonged period of partial bladder outlet obstruction (pBOO) in an animal model with physiologically relevant pBOO. Healthy, adult, female Fischer rats underwent surgical creation of a pBOO for either 2, 4, 8, or 13 weeks and were compared with sham-operated rats. Urodynamic measurements were used to compare bladder volumes and pressure. Tissue was grossly analysed with light microscopy and bladder weights and thicknesses were compared. Reverse transcription-polymerase chain reaction for collagen, transforming growth factor β (TGF-β), connective tissue growth factor (CTGF), hypoxia inducible factor 1α (HIF-1α), and platelet-derived growth factor (PDGF-A) was performed on all samples, as well as immunohistochemistry (IHC) for α-smooth muscle actin (α-SMA). Finally, mass spectrometry was used to quantify the collagen content of the bladders as a measure of fibrosis. After induction of pBOO, all rats remained healthy. Initial urodynamics showed an increase in capacity while maintaining normal pressures, but then deteriorated into small capacity, high-pressure bladders. Haematoxylin and eosin (H&E) staining showed an initial inflammatory response, and this was confirmed with significantly increased mRNA levels of TGF-β, CTGF, HIF-1α, and PDGF. The progression to smooth muscle hypertrophy was evident on H&E and confirmed with increased bladder mass and thickness. IHC for α-SMA showed a progressive increase associated with the elevated bladder pressures. Masson's trichrome and mass spectrometry showed a progressive increase in collagen to 13 weeks. With this model, we have effectively replicated the clinical scenario, with significant pathophysiological changes occurring insidiously in otherwise healthy rats. We believe that our observed changes represent distinct phases of bladder decompensation; with an initial inflammatory response to the stress of the pBOO, smooth muscle hypertrophy to overcome the increased urethral resistance, and eventual decompensation to fibrosis. The time course of the inflammatory markers implies the need for early intervention to prevent this cascade. Novel strategies targeting these observed physiological responses could lead to improved preventative strategies, with respect to biochemical pathways and the time course of their initiation. © 2010 THE AUTHORS. JOURNAL COMPILATION © 2010 BJU INTERNATIONAL.
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                Author and article information

                Contributors
                jlhbosch@xs4all.nl
                Journal
                Neurourol Urodyn
                Neurourol. Urodyn
                10.1002/(ISSN)1520-6777
                NAU
                Neurourology and Urodynamics
                John Wiley and Sons Inc. (Hoboken )
                0733-2467
                1520-6777
                06 July 2019
                December 2019
                : 38
                : Suppl 5 ( doiID: 10.1002/nau.v38.S5 )
                : S56-S65
                Affiliations
                [ 1 ] Department of Urology University Medical Centre Utrecht Utrecht The Netherlands
                [ 2 ] Department of Urology Bristol Urological Institute Bristol United Kingdom
                [ 3 ] Department of Urology Moinhos de Vento Hospital Porto Alegre Brazil
                [ 4 ] Department of Experimental Medicine and Surgery, Department of Surgery, Policlinico Tor Vergata University of Rome “Tor Vergata” and Urology Unit Rome Italy
                [ 5 ] Bristol Urological Institute Southmead Hospital Bristol United Kingdom
                [ 6 ] Department of Urology Maastricht University Medical Centre Maastricht The Netherlands
                [ 7 ] Department of Urology Guy's and St Thomas’ NHS Trust London United Kingdom
                Author notes
                [*] [* ] Correspondence Ruud Bosch, Department of Urology, University Medical Centre Utrecht, Utrecht 855500, 3508GA, The Netherlands.

                Email: jlhbosch@ 123456xs4all.nl

                Author information
                http://orcid.org/0000-0003-4833-0538
                http://orcid.org/0000-0002-8127-7153
                http://orcid.org/0000-0002-0308-8824
                http://orcid.org/0000-0001-5546-357X
                http://orcid.org/0000-0003-4823-1062
                http://orcid.org/0000-0003-4382-0394
                Article
                NAU24076
                10.1002/nau.24076
                6915908
                31278801
                c8f22da8-c5b7-41f3-a853-2ddea6cc6fbd
                © 2019 The Authors. Neurourology and Urodynamics Published by Wiley Periodicals, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 05 February 2019
                : 27 May 2019
                Page count
                Figures: 2, Tables: 2, Pages: 10, Words: 5382
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                December 2019
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.7.3 mode:remove_FC converted:17.12.2019

                Urology
                bladder dysfunction,bladder outlet obstruction,detrusor contractility,overactive bladder,underactive bladder

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