Premium
Functional and molecular characterisation of the bilateral pelvic nerve crush injury rat model for neurogenic detrusor underactivity
Author(s) -
Dewulf Karel,
Weyne Emmanuel,
Gevaert Thomas,
Deruyver Yves,
Voets Thomas,
Ridder Dirk De,
Everaerts Wouter,
Albersen Maarten
Publication year - 2019
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/bju.14649
Subject(s) - cystometry , urinary bladder , urology , medicine , urination , denervation , detrusor muscle , overactive bladder , in vivo , contractility , anesthesia , endocrinology , pathology , urinary system , biology , alternative medicine , microbiology and biotechnology
Objectives To create a rat model for neurogenic detrusor underactivity ( DU ) by bilateral pelvic nerve crush injury ( BPNI ) and to study temporal changes in detrusor contractility and morphology. Materials and Methods Male Sprague‐Dawley rats were subjected to BPNI or sham surgery and evaluated at 1, 3 and 9 weeks after surgery. Bladder function was determined in vivo by awake cystometry, micturition pattern analysis, and 24‐h urine collection. Bladders were harvested for in vitro pharmacological investigation by isometric tension recording. Bladders and major pelvic ganglia were investigated by quantitative reverse transcription‐polymerase chain reaction and histochemistry. Results Overflow incontinence was observed at 1 week after BPNI . At 3 and 9 weeks after BPNI , rats showed a bladder phenotype characteristic for DU with increased post‐void residual urine volumes, reduced voiding efficiencies, and lower maximum pressures. In isolated bladder strips, contractile responses to KC l, carbachol, and α,β‐methylene adenosine 5′‐triphosphate (α,β‐ mATP ) were preserved. On the other hand, neural‐induced contractility was reduced after BPNI , in line with reduced expression of protein gene product 9.5 and choline acetyltransferase in the major pelvic ganglion at 1 week after BPNI . The bladder‐to‐body weight ratio and detrusor thickness increased after BPNI , indicating detrusor hypertrophy to compensate for the reduced neural input. Conclusions BPNI induces a rat model for neurogenic DU . In this model, the detrusor maintains its contractility but denervation of the detrusor was observed.