A S Lin1, S Carrier, D M Morgan, T F Lue. 1. Department of Urology, University of California School of Medicine, San Francisco 94143-0738, USA.
Abstract
OBJECTIVES: To examine the effect of simulated birth injury in an animal model as part of a study on the pathogenesis of stress urinary incontinence (SUI) and the urinary continence mechanism. METHODS: A balloon was inflated in the vaginas of rats for 4 hours to simulate prolonged labor. The effect on the continence mechanism was assessed by functional, anatomic, biochemical, and histologic examinations. The functional test consisted of placing chili powder or a clipped whisker into the rat's nostrils to induce sneezing. Anatomic measurement of the genital hiatus was performed with a caliper. Serum creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were measured to examine the value of muscle injury in predicting incontinence. c-Fos immunostaining in the spinal cord was used as a marker of nerve injury. These data were then correlated with histopathologic examination of the urethra and pelvic floor tissues. RESULTS: Four weeks after simulated birth injury, SUI was noted in 19 of 48 experimental rats. The genital hiatus was significantly wider in incontinent rats. The serum CPK and LDH levels were markedly elevated, but no difference was noted between the continent and incontinent rats. All experimental rats showed many c-Fos immunostaining neurons in the L6 to S1 spinal cord segments, but none was seen in control rats. Histologic study revealed a marked decrease of ganglion cells in the neural plexuses posterolateral to the vagina in experimental rats. After 4 weeks, muscle necrosis and degeneration, irregular shape and size of muscle fibers, and a change in the type I/II ratio were prominent features in the levator ani. In the urethra, we noted a significant decline in urethral wall musculature (both smooth and striated) in incontinent rats. CONCLUSIONS: In this novel rat model, simulated birth injury resulted in SUI in a portion of the animals. Pathologic changes in the urethra, pelvic ganglia, and levator muscles seem to be the contributing factors to SUI.
OBJECTIVES: To examine the effect of simulated birth injury in an animal model as part of a study on the pathogenesis of stress urinary incontinence (SUI) and the urinary continence mechanism. METHODS: A balloon was inflated in the vaginas of rats for 4 hours to simulate prolonged labor. The effect on the continence mechanism was assessed by functional, anatomic, biochemical, and histologic examinations. The functional test consisted of placing chili powder or a clipped whisker into the rat's nostrils to induce sneezing. Anatomic measurement of the genital hiatus was performed with a caliper. Serum creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were measured to examine the value of muscle injury in predicting incontinence. c-Fos immunostaining in the spinal cord was used as a marker of nerve injury. These data were then correlated with histopathologic examination of the urethra and pelvic floor tissues. RESULTS: Four weeks after simulated birth injury, SUI was noted in 19 of 48 experimental rats. The genital hiatus was significantly wider in incontinent rats. The serum CPK and LDH levels were markedly elevated, but no difference was noted between the continent and incontinent rats. All experimental rats showed many c-Fos immunostaining neurons in the L6 to S1 spinal cord segments, but none was seen in control rats. Histologic study revealed a marked decrease of ganglion cells in the neural plexuses posterolateral to the vagina in experimental rats. After 4 weeks, muscle necrosis and degeneration, irregular shape and size of muscle fibers, and a change in the type I/II ratio were prominent features in the levator ani. In the urethra, we noted a significant decline in urethral wall musculature (both smooth and striated) in incontinent rats. CONCLUSIONS: In this novel rat model, simulated birth injury resulted in SUI in a portion of the animals. Pathologic changes in the urethra, pelvic ganglia, and levator muscles seem to be the contributing factors to SUI.
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