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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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Systemic atherosclerosis causes detrusor overactivity: functional and morphological changes in hyperlipoproteinemic
Thomas Bschleipfer1, Anne-Kathrin Dannenmaier1, Christian Illig1
1Department of Urology, Pediatric Urology and Andrology, Universitätsklinikum Giessen und Marburg GmbH, Giessen, Justus-Liebig University Giessen, Giessen, Germany.
The Journal of Urology
|August 31, 2014
Summary
Systemic atherosclerosis in mice models is linked to detrusor overactivity, a bladder dysfunction. Reduced bladder vascularization and inflammation appear to be key factors in its development.
Area of Science:
- Cardiovascular Biology
- Urology
- Vascular Biology
Background:
- Systemic atherosclerosis and overactive bladder increase with age.
- An association between these conditions has not been established.
- Atherosclerosis is an inflammatory disease.
Purpose of the Study:
- To investigate the link between systemic atherosclerosis and bladder dysfunction.
- To evaluate bladder function and morphology in a mouse model of atherosclerosis.
- To explore the role of vascularization in atherosclerosis-induced detrusor overactivity.
Main Methods:
- Cystometry was performed on 60-week-old apoE(-/-)LDLR(-/-) mice and controls.
- Bladders were analyzed using nano-computerized tomography and 3D reconstruction.
- Histomorphological analysis examined bladder tissue and vascular structures.
Main Results:
- ApoE(-/-)LDLR(-/-) mice showed decreased bladder capacity and voiding intervals.
- Maximum bladder pressure increased in the atherosclerosis model.
- Reduced bladder wall thickness, vascular volume, and vascularity were observed.
- Intramural vessels had thickened media, and inflammatory cells were present.
Conclusions:
- This study presents a novel mouse model for nonneurogenic detrusor overactivity due to atherosclerosis.
- Decreased bladder vascularization is a significant factor in detrusor overactivity onset.
- Atherosclerosis-related inflammation may contribute to detrusor overactivity.
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