Huang Jian, Cheng Mingjun, Ding Yan, Chen Limei, Hua Keqin
Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.
J Obstet Gynaecol Res. 2013 Jan;39(1):256-63. doi: 10.1111/j.1447-0756.2012.01959.x. Epub 2012 Jul 29.
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.
本研究旨在建立一种改良的大鼠产后压力性尿失禁（SUI）模型，该模型易于构建，并能稳定地评估尿动力学变化。
将导尿管插入40只大鼠的阴道，充盈球囊8小时以模拟分娩。将一根胡须插入鼻孔诱发打喷嚏。通过测量漏点压力（LPP）和最大膀胱容量，观察阴道扩张或打喷嚏引起的尿动力学变化。检测血清乳酸脱氢酶（LDH）和肌酸激酶（CK），并测量耻骨尾骨肌组织中半胱天冬酶-3的mRNA表达，以显示SUI中肌肉损伤的影响。
阴道球囊扩张8小时后，建立了产后SUI大鼠模型，成功率为72.5%（29/40）。通过喷嚏试验，分别在第1、7、14、28和56天观察到100%（5/5）、80%（4/5）、60%（3/5）、60%（3/5）和40%（2/5）的实验大鼠出现SUI。对照组（n = 10）未发现SUI。这29只实验大鼠的血清LDH和CK水平最初升高，在第7天达到峰值，最终降至正常水平。与对照大鼠相比，差异有统计学意义（P < 0.05）。实验大鼠耻骨尾骨肌中半胱天冬酶-3基因的表达在第1天达到峰值，此后下降，而对照组未见此变化，差异有统计学意义（P < 0.05）。
阴道球囊扩张8小时可导致该大鼠模型出现SUI。血清LDH和CK以及肌肉凋亡基因的变化与人类产后SUI患者相似。因此，它可被视为研究产后SUI发病机制的有用动物模型。
