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A Decentralized Ex Vivo Murine Bladder Model with the Detrusor Muscle Removed for Direct Access to the Suburothelium during Bladder Filling
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Luminal DMSO: effects on detrusor and urothelial/lamina propria function
Katrina J Smith1, Russ Chess-Williams1, Catherine McDermott1
1Faculty of Health Sciences & Medicine, Bond University, Gold Coast, QLD 4229, Australia.
Biomed Research International
|June 21, 2014
Summary
Dimethyl sulfoxide (DMSO) treatment for interstitial cystitis can cause bladder urothelial damage, leading to mediator release and altered bladder function, potentially explaining symptom flare-ups.
Area of Science:
- Urology
- Pharmacology
- Cell Biology
Background:
- Dimethyl sulfoxide (DMSO) is a topical treatment for interstitial cystitis (IC), a chronic bladder condition.
- The precise mechanisms by which DMSO affects bladder function and histology in IC are not fully understood.
Purpose of the Study:
- To investigate the effects of luminal DMSO application on porcine bladder urothelium and detrusor muscle.
- To assess the release of key mediators like ATP and acetylcholine (Ach) and their impact on bladder contractility.
Main Methods:
- Porcine bladders were treated with 50% DMSO on the luminal surface.
- Release of ATP, acetylcholine, and lactate dehydrogenase (LDH) was measured.
- Histological examination assessed urothelial integrity.
- Contractile responses of bladder strips to carbachol and electrical field stimulation were evaluated.
Main Results:
- Luminal DMSO induced the release of ATP, Ach, and LDH, with histological evidence of urothelial damage.
- DMSO pretreatment reduced ATP and Ach release from urothelial/lamina propria strips but enhanced carbachol-induced contractions.
- The urothelium's inhibitory effect on detrusor contraction was diminished after DMSO treatment.
- Neurogenic responses to electrical field stimulation were enhanced in DMSO-treated bladders.
Conclusions:
- DMSO permeabilizes urothelial membranes, causing leakage of intracellular mediators.
- Enhanced bladder contractility and mediator release are consistent with the initial symptom flare-ups observed in IC patients post-DMSO treatment.
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