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Evidence of increased centrally enhanced bladder compliance with ageing in a mouse model
Author(s) -
Smith Phillip P.,
DeAngelis Anthony,
Simon Richard
Publication year - 2015
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.12669
Subject(s) - compliance (psychology) , cystometry , medicine , ageing , urination , urinary bladder , concomitant , urinary system , urology , psychology , social psychology
Objective To test the hypothesis that ageing is associated with increasing neurogenic enhancement of bladder filling compliance. Materials and Methods Female B 6 mice (aged 2, 12, 22 and 26 months) underwent cystometry while alive and immediately after death. Bladder compliance was calculated from pressure‐time data. Pressure data were transformed using F ast F ourier T ransform to obtain power spectra of bladder pressure variations attributable to contractile activity during filling in both alive and dead mice. A cut‐off frequency ( CF ) was determined for each mouse, above which any power content would be primarily neurogenic. Compliance and power spectra results were compared among age groups, and correlations sought. Results A reversible loss of bladder compliance and non‐voiding contractile ( NVC ) activity followed abolition of voiding reflexes in female colony mice in all age groups. Bladder filling compliance increased with age in urethane‐anaesthetised and post‐mortem conditions, and more so in the former. Power below the CF did not significantly vary with age. Neurogenic power increased with age, and significantly correlated with compliance. Conclusions An increase in neurogenic power during filling accompanies increased centrally mediated compliance enhancement with age. A bladder control model in which brain processes related to micturition may compensate for age‐associated changes; thereby preserving voiding function is suggested. Urinary dysfunction could be viewed as the result of homeostatic failure rather than strictly end‐organ pathology.