大鼠产后压力性尿失禁模型的建立与探讨

目的 应用在大鼠阴道内放置水囊模拟产伤破坏大鼠盆底组织的方法建立产后压力性尿失禁( postpartum urinary incontinence,PPUI)的动物模型,并对此模型进行初步研究.方法 对40只SD雌性大鼠进行持续8h水囊扩张阴道,随机选取PPUI模型建立成功的大鼠25只并与对照同龄大鼠5只分别于模型建立后1d、1周、2周、4周、8周进行喷嚏实验以及尿动力学测定,张力换能器测定盆底肌肉肌力强度,采用JSCC标准化对应法测定血清生化指标(LDH,CK),应用逆转录-聚合酶链反应检测caspase-3基因表达,胆碱酯酶染色法计数盆底肌肉乙酰胆碱受体数量.结果 建模后喷嚏实验阳性率明显升高,阳性率为72.5％(29/40),尿动力学检测最大膀胱容量及漏尿点压力均降低,盆底肌肉收缩力下降,血清LDH、CK水平上升,盆底耻尾肌乙酰胆碱受体数量减少,与对照组比较均差异有显著性(P＜0.05).耻尾肌组织中caspase-3基因表达在建立模型当日达到最高,与对照组差异有显著性(P＜0.05),之后逐渐下降.结论 大鼠阴道内放置8h水囊的方法可以成功模拟产后压力性尿失禁,引起尿动力以及盆底肌肉的相关损伤指标发生改变.

Establishment and characterization of a rat model of postpartum stress urinary incontinence

Objective To establish a rat model of postpartum stress urinary incontinence（PPUI） through vaginal placement of urinary catheter balloon causing pelvic organ injury.Methods After the vaginal catheter balloon dilation for 8 hours on 40 Sprague-Dawley female rats,25 were randomly selected as experimental group and 5 normal rats of the same age as control group.Sneeze test was used on the day of the procedure and on weeks 1,2,4 and 8.The animal models were evaluated through urodynamics as measured by leak point pressure（LPP）,maximum bladder volume,pelvic floor muscle acetylcholine receptor content,comparison of serum lactate dehydrogenase（LDH） and creatine kinase（CK） according to the JSCC standards,pelvic floor muscle strength and RT-PCR assessment of caspase-3 expression.Results After 8 hours of vaginal balloon dilation,a rat model of PPUI was established with a success rate of 72.5%（29/40）.In the model animals,LDH and CK were initially increased,peaked on day 7,and finally decreased toward normal values.The pelvic floor muscle contraction strength and pelvic pubococcygeus acetylcholine receptors were declined.There were significant differences in the values between experimental and control groups（P0.05）.Pubococcygeal muscle caspase-3 gene expression peaked on the day of the procedure（P0.05） and decreased thereafter.Conclusions Rats subjected to vaginal balloon dilation for 8 hours display biochemical alterations in sera,activation of caspase-3,and decreased pelvic floor muscle contraction strength,similar to those observed in human PPUI patients.