| Objective:1 To investigate the methods of establishing the stress urinary incontinence (SUI)model of rats; 2 To determine both the distribution and expression of non-adrenergic and non-cholinergic neurotransmitters(NANC) nitric oxide (NO) and vasoactive intestinal peptide (VIP) in the urethra, vagina, levator ani muscle.of model rats 3 To clarify their roles in the pathogenesis of SUI, and provide valuable basis for in-depth study and neurotransmitters treatment.Methods:50 Sprague-Dawley rats were fed in the same cage(male to female is 4:1), After delivery, all female rats were randomly divided into two groups. The first group was 12 rats and the second group was 28. The first group rats were fed regularly, without any special treatment during the whole breeding. Every rat in the second group had been overspread the vagina with the air balloon for 4 hours to simulate the vaginal delivery trauma. Two weeks later, the rats were repeated the same operation again. After this, ovariectomy was performed on each and bred conventionally for eight weeks. Then the urodynamic test was done, including the maximum bladder capacity (MBC), the abdominal leak point pressure (ALPP) and the sneeze test. According to the urodynamic results,12 female rats were randomly chosen as stress urinary incontinence (SUI) models. The other 12 normal femal rats were chosen from the first group as the control group. All the rats were sacrificed and the urethra, vagina and levator ani muscle were taken to do the HE staining and to do the immunohistochemical examination to detect the distribution and the differential expression of nitric oxide (NO) and vasoactive intestinal peptide (VIP) in the urethra, vagina and levator ani muscle.Results:(1):The modified abdominal leak point pressure of the controlled group and experimental group were (48.00±1.74) cmH2O and (32.94±1.63) cmH2O, the statistical difference was significant (P<0.05); the maximum cystometries were (2.02±0.19) ml and (1.29±0.16) ml, the difference was significant (P<0.05) and the positive rates of model rat was 13/15(52%), All of the control rats were negative. (2)The urethra, vagina, levator ani muscle of control group shows uniform staining, cell size of normal muscle fibers arranged regularly in HE staining. However, in HE staining, the uneven staining, tissue edema, atrophy thinning, muscle fiber loosely arranged and slightly disordered were showed in the experimental group. A small amount of inflammation and cell necrosis were seen in the experimental group too. (3) the immunohistochemical staining showed that the Integrated optical density of nitric oxide (NO) in the urethra, vagina, levator ani muscle was 3.95±1.02,6.01±1.32 and18.67±4.94 In controlled group. And in the experimental group was1.04±0.38,1.44±0.48,6.16±1.32. Integrated optical density of vasoactive intestinal peptide (VIP) was 3.57±0.77,7.15±1.67,20.29±3.39.in the controlled group and 0.73±0.23,2.51±0.60,3.69±1.24.in the experimental group The results of nitric oxide (NO) and vasoactive intestinal peptide (VIP) in the urethra, vagina, levator ani muscleNO and VIP have the statistical significance in the controlled and experimental groups.Conclusions:(1)Stress urinary incontinence rats model can be successfully established by vagina balloon dilatation combined with ovariectomy. (2) pelvic floor muscle degeneration, edema may weaken the pelvic floor and may be one of the reason of the pathogenesis of SUI. (3) The non-adrenergic non-cholinergic neurotransmitter nitric oxide (NO) and vasoactive intestinal peptide (VIP) changes in the urethra, vagina, levator ani muscle in the experimental group and control group indicating that neurotransmitters may play a role in the development of SUI.
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