Lin A S, Carrier S, Morgan D M, Lue T F
Department of Urology, University of California School of Medicine, San Francisco 94143-0738, USA.
Urology. 1998 Jul;52(1):143-51. doi: 10.1016/s0090-4295(98)00136-8.
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.
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.
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.
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.
作为压力性尿失禁（SUI）发病机制及尿失禁机制研究的一部分，在动物模型中研究模拟分娩损伤的影响。
在大鼠阴道内充气球4小时以模拟产程延长。通过功能、解剖、生化和组织学检查评估对尿失禁机制的影响。功能测试包括将辣椒粉或剪断的胡须放入大鼠鼻孔以诱发打喷嚏。用卡尺对生殖裂孔进行解剖测量。测量血清肌酸磷酸激酶（CPK）和乳酸脱氢酶（LDH）以检查肌肉损伤在预测尿失禁方面的价值。脊髓中的c-Fos免疫染色用作神经损伤的标志物。然后将这些数据与尿道和盆底组织的组织病理学检查结果相关联。
模拟分娩损伤四周后，48只实验大鼠中有19只出现SUI。尿失禁大鼠的生殖裂孔明显更宽。血清CPK和LDH水平显著升高，但尿失禁大鼠和非尿失禁大鼠之间无差异。所有实验大鼠在L6至S1脊髓节段均显示许多c-Fos免疫染色神经元，而对照大鼠中未见。组织学研究显示，实验大鼠阴道后外侧神经丛中的神经节细胞明显减少。四周后，肛提肌中肌肉坏死和变性、肌纤维形状和大小不规则以及I型/II型比例变化是突出特征。在尿道中，我们注意到尿失禁大鼠的尿道壁肌肉组织（平滑肌和横纹肌）显著减少。
在这个新的大鼠模型中，模拟分娩损伤导致部分动物出现SUI。尿道、盆腔神经节和肛提肌的病理变化似乎是导致SUI的因素。
