Beverley Greenwood-Van Meerveld1, Ehsan Mohammadi2, Karl Tyler2, Samuel Van Gordon3, Alex Parker4, Rheal Towner5, Robert Hurst6. 1. Veterans Affairs Medical Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; University of Oklahoma College of Medicine, Oklahoma City, Oklahoma. Electronic address: beverley-greenwood@ouhsc.edu. 2. Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; University of Oklahoma College of Medicine, Oklahoma City, Oklahoma. 3. Department of Urology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; University of Oklahoma College of Medicine, Oklahoma City, Oklahoma. 4. University of Oklahoma College of Medicine, Oklahoma City, Oklahoma. 5. Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma. 6. Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; Department of Urology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; University of Oklahoma College of Medicine, Oklahoma City, Oklahoma.
Abstract
PURPOSE: The pathophysiology of painful bladder syndrome is poorly understood. However, there is evidence of female predominance and comorbidity with irritable bowel syndrome. Our hypothesis is that cross-sensitization between bladder and colon is due to altered permeability in 1 organ, which affects the other organ. MATERIALS AND METHODS: Experiments were performed in anesthetized, ovariectomized female rats. In separate groups protamine sulfate was infused in the bladder or trinitrobenzene sulfonic acid was infused in the colon. Untreated rats served as controls. Bladder and colonic tissue were harvested from all rats 1, 3 and 5 days after treatment. Permeability was assessed in vitro in Ussing chambers by measuring transepithelial electrical resistance and macromolecular flux of fluorescein isothiocyanate-dextran. RESULTS: Exposing the bladder to protamine sulfate induced a significant decrease in bladder transepithelial electrical resistance and an increase in the translocation of fluorescein isothiocyanate across the tissue compared to controls at 1 and 3 days (p <0.05). Colonic tissue from rats with enhanced bladder permeability showed a significant decrease in transepithelial electrical resistance and increase in fluorescein isothiocyanate compared to untreated controls at all time points (p <0.05). Conversely when colonic permeability was increased with trinitrobenzene sulfonic acid, we observed an increase in bladder permeability in the absence of any changes to the bladder urothelium. CONCLUSIONS: Changes in epithelial permeability may represent a novel mechanism for visceral organ crosstalk. It may explain the overlapping symptomology of painful bladder syndrome and irritable bowel syndrome.
PURPOSE: The pathophysiology of painful bladder syndrome is poorly understood. However, there is evidence of female predominance and comorbidity with irritable bowel syndrome. Our hypothesis is that cross-sensitization between bladder and colon is due to altered permeability in 1 organ, which affects the other organ. MATERIALS AND METHODS: Experiments were performed in anesthetized, ovariectomized female rats. In separate groups protamine sulfate was infused in the bladder or trinitrobenzene sulfonic acid was infused in the colon. Untreated rats served as controls. Bladder and colonic tissue were harvested from all rats 1, 3 and 5 days after treatment. Permeability was assessed in vitro in Ussing chambers by measuring transepithelial electrical resistance and macromolecular flux of fluorescein isothiocyanate-dextran. RESULTS: Exposing the bladder to protamine sulfate induced a significant decrease in bladder transepithelial electrical resistance and an increase in the translocation of fluorescein isothiocyanate across the tissue compared to controls at 1 and 3 days (p <0.05). Colonic tissue from rats with enhanced bladder permeability showed a significant decrease in transepithelial electrical resistance and increase in fluorescein isothiocyanate compared to untreated controls at all time points (p <0.05). Conversely when colonic permeability was increased with trinitrobenzene sulfonic acid, we observed an increase in bladder permeability in the absence of any changes to the bladder urothelium. CONCLUSIONS: Changes in epithelial permeability may represent a novel mechanism for visceral organ crosstalk. It may explain the overlapping symptomology of painful bladder syndrome and irritable bowel syndrome.
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