Journal article

Systemic Atherosclerosis Causes Detrusor Overactivity: Functional and Morphological Changes in Hyperlipoproteinemic apoE-/- LDLR-/- Mice


Authors listBschleipfer, Thomas; Dannenmaier, Anne-Kathrin; Illig, Christian; Kreisel, Melanie; Gattenloehner, Stefan; Langheinrich, Alexander C.; Krombach, Gabriele A.; Weidner, Wolfgang; Kampschulte, Marian

Publication year2015

Pages345-351

JournalThe Journal of Urology

Volume number193

Issue number1

ISSN0022-5347

eISSN1527-3792

DOI Linkhttps://doi.org/10.1016/j.juro.2014.08.098

PublisherLippincott, Williams & Wilkins


Abstract

Purpose: The prevalence of systemic atherosclerosis and overactive bladder/detrusor overactivity increases almost simultaneously with age but an association between these diseases has not yet been proved. We evaluated changes in bladder function and morphology, including vascularization, in apoE(-/-) LDLR-/- double knockout mice with systemic atherosclerosis but without central nervous system involvement.

Materials and Methods: Cystometry was performed in awake, freely moving 60-week-old apoE(-/-) LDLR-/- mice and C57BL/6N controls. The mice were sacrificed and perfused with Microfil (R) contrast medium. The bladder was excised, dissected and scanned by nano-computerized tomography, including 3-dimensional reconstruction. Samples then underwent histomorphological analysis.

Results: In apoE(-/-) LDLR-/- mice cystometry revealed a significant decrease in the peak-peak interval, micturition interval, functional bladder capacity and micturition volume. However, maximum bladder pressure increased. Nano-computerized tomography revealed a significant reduction in bladder wall thickness, segment volume, vascular volume and the vascular volume fraction. Histomorphologically bladder specimens showed a thickened media of intramural vessels, activated endothelial cells and intramural inflammatory cells.

Conclusions: To our knowledge this study presents a new in vivo mouse model of nonneurogenic detrusor overactivity caused by systemic atherosclerosis. Decreased bladder wall vascularization seems to be a major factor for detrusor overactivity onset. Capillaries are rarified with reduced lumina due to thickened media. Activated endothelial cells and the infiltration of inflammatory cells in apoE(-/-) LDLR-/- mice underlines once more that atherosclerosis is an inflammatory process that may also be relevant to the onset of detrusor overactivity.




Citation Styles

Harvard Citation styleBschleipfer, T., Dannenmaier, A., Illig, C., Kreisel, M., Gattenloehner, S., Langheinrich, A., et al. (2015) Systemic Atherosclerosis Causes Detrusor Overactivity: Functional and Morphological Changes in Hyperlipoproteinemic apoE-/- LDLR-/- Mice, The Journal of Urology, 193(1), pp. 345-351. https://doi.org/10.1016/j.juro.2014.08.098

APA Citation styleBschleipfer, T., Dannenmaier, A., Illig, C., Kreisel, M., Gattenloehner, S., Langheinrich, A., Krombach, G., Weidner, W., & Kampschulte, M. (2015). Systemic Atherosclerosis Causes Detrusor Overactivity: Functional and Morphological Changes in Hyperlipoproteinemic apoE-/- LDLR-/- Mice. The Journal of Urology. 193(1), 345-351. https://doi.org/10.1016/j.juro.2014.08.098



Keywords


BLADDER FUNCTIONInfarctionLOWER URINARY-TRACTmodels, animalRAT MODELSTANDARDIZATION SUB-COMMITTEEtomography, emission-computedurinary bladder, overactiveVASA VASORUM NEOVASCULARIZATION


SDG Areas


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