Prantil Rachelle L, Jankowski Ron J, Kaiho Yasuhiro, de Groat William C, Chancellor Michael B, Yoshimura Naoki, Vorp David A
Depts. of Surgery and Bioengineering, Suite 200, Bridgeside Point, McGowan Institute for Regenerative Medicine, 100 Technology Dr., Pittsburgh, PA 15219, USA.
Am J Physiol Renal Physiol. 2007 Apr;292(4):F1229-37. doi: 10.1152/ajprenal.00292.2006. Epub 2006 Dec 26.
Stress urinary incontinence (SUI) is the involuntary release of urine during sudden increases in abdominal pressures. SUI is common in women after vaginal delivery or pelvic trauma and may alter the biomechanical properties of the urethra. Thus we hypothesize that injury due to vaginal distension (VD) decreases urethral basal tone and passive stiffness. This study aimed to assess the biomechanical properties of the urethra after VD in the baseline state, where basal muscle tone and extracellular matrix (ECM) are present, and in the passive state, where inactive muscle and ECM are present. Female rat urethras were isolated in a rat model of acute SUI induced by simulated birth trauma. Our established ex vivo system was utilized, wherein we applied intraluminal static pressures ranging from 0 to 20 mmHg. Outer diameter was measured via a laser micrometer. Measurements were recorded via computer. Urethral thickness was assessed histologically. Stress-strain responses of the urethra were altered by VD. Quantification of biomechanical parameters indicated that VD decreased baseline stiffness. The passive peak incremental elastic modulus of the distal segment in VD urethras was less than for controls (1.84 +/- 0.67 vs. 1.19 +/- 0.70 x 10(6) dyne/cm(2), respectively; P = 0.016). An increase was noted in passive low-pressure compliance values in proximal VD urethras compared with controls (9.44 +/- 2.43 vs. 4.62 +/- 0.60 mmHg(-1), respectively; P = 0.04). Biomechanical analyses suggest that VD alters urethral basal tone, proximal urethral compliance, and distal stiffness. Lack of basal smooth muscle tone, in combination with these changes in the proximal and distal urethra, may contribute to SUI induced by VD.
压力性尿失禁(SUI)是指在腹压突然增加时出现的不自主漏尿。SUI在阴道分娩或盆腔创伤后的女性中很常见,并且可能改变尿道的生物力学特性。因此,我们推测阴道扩张(VD)导致的损伤会降低尿道的基础张力和被动硬度。本研究旨在评估在存在基础肌张力和细胞外基质(ECM)的基线状态以及存在非活性肌肉和ECM的被动状态下,VD后尿道的生物力学特性。在由模拟分娩创伤诱导的急性SUI大鼠模型中分离雌性大鼠尿道。使用我们建立的离体系统,在该系统中我们施加0至20 mmHg的腔内静态压力。通过激光测微仪测量外径。测量结果通过计算机记录。通过组织学评估尿道厚度。VD改变了尿道的应力-应变反应。生物力学参数的量化表明VD降低了基线硬度。VD尿道远端节段的被动峰值增量弹性模量低于对照组(分别为1.84±0.67与1.19±0.70×10(6)达因/厘米(2);P = 0.016)。与对照组相比,近端VD尿道的被动低压顺应性值有所增加(分别为9.44±2.43与4.62±0.60 mmHg(-1);P = 0.04)。生物力学分析表明,VD改变了尿道的基础张力、近端尿道顺应性和远端硬度。基础平滑肌张力的缺乏,与近端和远端尿道的这些变化相结合,可能导致VD诱发的SUI。