Abstract

The aim of this study was to develop a modified rat model for postpartum stress urinary incontinence (SUI) which can be easily established and which will steadily evaluate urodynamic changes. A urinary catheter was placed into the vaginas of rats (n=40) and the balloon was inflated for 8 h to simulate labor. A whisker was inserted into the nostril to induce sneezing. The urodynamic changes induced by vaginal dilation or sneezing were observed by measurement of leak point pressure (LPP), and maximum bladder volume. Serum lactose dehydrogenase (LDH) and creatine kinase (CK) were tested, and the mRNA expression of caspase-3 in pubococcygeus muscle tissue was measured to show the effect of muscle injury in SUI. After 8 h of balloon vaginal dilation, a rat model of postpartum SUI was established with a success rate of 72.5% (29/40). By sneeze assay, SUI was noted in 100% (5/5), 80% (4/5), 60% (3/5), 60% (3/5) and 40% (2/5) of experimental rats on day 1, 7, 14, 28 and 56, respectively. No SUI was found in the control group (n=10). The level of serum LDH and CK in these 29 experimental rats initially increased, peaked on day 7, and finally decreased toward normal values. Compared with control rats, the differences were significant (P<0.05). The expression of the caspase-3 gene in pubococcygeal muscle of experimental rats peaked on day 1 and decreased thereafter, while no such change was seen in the control group, and the difference was significant (P<0.05). Eight hours of vaginal balloon dilation resulted in SUI in this rat model. The alterations in serum LDH and CK, and in the muscle's apoptotic genes mimic those observed in human postpartum SUI patients. It can therefore be considered as a useful animal model for the study on the pathogenesis of postpartum SUI.

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