MP1-02 UNDERSTANDING THE MECHANISMS OF VISCERAL ORGAN CROSSTALK: IS IT ALL DUE TO ALTERED PERMEABILITY?

Abstract

You have accessJournal of UrologyUrodynamics/Incontinence/Female Urology: Basic Research I1 Apr 2014MP1-02 UNDERSTANDING THE MECHANISMS OF VISCERAL ORGAN CROSSTALK: IS IT ALL DUE TO ALTERED PERMEABILITY? Ehsan Mohammadi, Karl Tyler, William Dakil, Samuel VanGordon, Beverley Greenwood-Van Meerveld, and Robert Hurst Ehsan MohammadiEhsan Mohammadi More articles by this author , Karl TylerKarl Tyler More articles by this author , William DakilWilliam Dakil More articles by this author , Samuel VanGordonSamuel VanGordon More articles by this author , Beverley Greenwood-Van MeerveldBeverley Greenwood-Van Meerveld More articles by this author , and Robert HurstRobert Hurst More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.100AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Although the pathophysiology of painful bladder syndrome (PBS) is poorly understood there is evidence of female predominance and comorbidity with irritable bowel syndrome (IBS). It is our hypothesis that altered bladder permeability leads to hyperexcitability of visceral afferent neurons and underlies pelvic organ cross sensitization. In this study we aimed to investigate the effect of acute bladder damage on the permeability of the bladder and colon. METHODS Experiments were performed in anesthetized, ovariectomized (OVX) female Sprague Dawley rats (n = 28); the bladder was catheterized for the intravesical administration of protamine sulfate (1mg/ml in 400 μl) saline-instilled and untreated naïve rats served as controls. After 24 hr. the bladder and colonic tissue were harvested. A sample was taken for histology and the remaining tissue was mounted into modified Ussing chambers and bathed in Kreb’s solution at 37°C. After a stabilization period, permeability was assessed electrophysiologically via transepithelial resistance (TEER) and via the flux of a macromolecular marker (fluorescein isothiocynate-dextrin [FITC-4 KD). RESULTS Other than mild edema, exposing the bladder to protamine sulfate induced very minimal physical urothelial damage but no colonic damage as defined histologically. We therefore conclude the main effect was to neutralize the protective glycosaminoglycan layer. However, there was a significant (P<0.01) decrease in TEER in protamine-sulfate treated bladders (1175 ± 164 ω/cm2) compared to saline-treated (1617 ± 202 1ω/cm2) or naïve controls (2524 ± 422 ω/cm2). We also found that in response to mild bladder damage, colonic TEER significantly (P<0.05) decreased (126.7 ± 22.44 ω/cm2) when compared to saline-treated (177.7 ± 14.23 ω/cm2) and untreated naïve controls (233.7 ± 14.14 ω/cm2). CONCLUSIONS These data demonstrate that following acute bladder damage there is not only an increase in bladder permeability but also a marked rise in the permeability of the colon in the absence of any histological damage to the colon. Thus changes in epithelial permeability may represent a novel mechanism for visceral organ crosstalk and may be important in the overlapping symptomology of PBS and IBS. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e1 Peer Review Report Advertisement Copyright & Permissions© 2014MetricsAuthor Information Ehsan Mohammadi More articles by this author Karl Tyler More articles by this author William Dakil More articles by this author Samuel VanGordon More articles by this author Beverley Greenwood-Van Meerveld More articles by this author Robert Hurst More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...