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1 Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States; Research Service, Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States
2 Anatomy and Cell Biology, Rush University, Chicago, Illinois, United States
3 Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio, United States; Research Service, Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States; Research Service, Hines VA Hospital, Hines, Illinois, United States
4 Research Service, Hines VA Hospital, Hines, Illinois, United States
* To whom correspondence should be addressed. E-mail: damasem{at}ccf.org.
Stress urinary incontinence (SUI) development is strongly correlated with vaginal childbirth, particularly increased duration of the 2nd stage of labor. However, the mechanisms of pelvic floor injury leading to SUI are largely unknown. The aim of this study was to determine the effects of increased duration of vaginal distension (VD) on voiding cystometry, leak point pressure testing and histology. Sixty-nine virgin female rats underwent VD using an inflated balloon for either 1 hour or 4 hours, while 33 age-matched rats were sham-VD controls. Conscious cystometry, leak point pressure testing and histopathology were determined 4 days, 10 days and 6 weeks after VD. The increase in abdominal pressure to leakage (LPP) during leak point pressure testing was significantly decreased in both distension groups 4 days after distension, indicative of short-term decreased urethral resistance. Ten days after VD, LPP was significantly decreased in the 4 hour but not the 1-hour distension group, indicating that a longer recovery time is needed following longer distension duration. Six weeks after VD, LPP was not significantly different from sham values, indicating a return toward normal urethral resistance. In contrast, 6 weeks after VD of either duration, the rats had not undergone the same increase in voided volume as the sham group, suggesting that some effects of VD do not resolve within 6 weeks. Both VD groups demonstrated histopathological evidence of acute injuries and tissue remodeling. In conclusion, this experiment suggests pressure-induced hypoxia as a possible mechanism of injury in vaginal delivery.
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