Department of Bioengineering, Sanford Consortium for Regenerative Medicine, University of California, San Diego, California.
Department of Orthopaedic Surgery, University of California, San Diego, California.
Neurourol Urodyn. 2019 Mar;38(3):912-919. doi: 10.1002/nau.23946. Epub 2019 Feb 19.
To define the operational resting sarcomere length (L ) of the female rat external urethral sphincter (EUS) and external anal sphincter (EAS) and to determine the mechanism of parturition-related injury of EUS and EAS using a simulated birth injury (SBI) vaginal distention model.
EUS and EAS of 3-month-old Sprague-Dawley control and injured rats were fixed in situ, harvested, and microdissected for L measurements and assessment of ultrastructure. EUS and EAS function was determined at baseline, and immediately and 4 weeks after SBI, using leak point pressure (LPP) and anorectal manometry (ARM), respectively. Operational L was compared to species-specific optimal L using one sample Student's t test. Data (mean ± SD) were compared between groups and time points using repeated measures one-way analysis of variance, followed by Tukey's post hoc pairwise comparisons, with significance set to 0.05.
The operational resting L of both sphincters (EUS: 2.09 ± 0.07 µm, EAS: 2.02 ± 0.03 µm) was significantly shorter than optimal rat L of 2.4 µm. Strains imposed on EUS and EAS during SBI resulted in significant sarcomere elongation and disruption, compared with the controls (EUS: 3.09 ± 0.11 µm, EAS: 3.37 ± 0.09 µm). Paralleling structural changes, LPP and ARM measures were significantly lower immediately (LPP: 21.5 ± 1.0 cmH O, ARM: 5.1 ± 2.31 cmH O) and 4 weeks (LPP: 27.7 ± 1.3cmH O, ARM: 2.5 ± 1.0 cmH O) after SBI relative to the baseline (LPP: 43.4 ± 8.5 cmH O, ARM: 8.2 ± 2.0 cmH O); P < 0.05.
Analogous to humans, the short resting L of rat EUS and EAS favors their sphincteric function. The insult experienced by these muscles during parturition leads to sarcomere hyperelongation, myofibrillar disruption, and dysfunction of the sphincters long-term.
定义雌性大鼠尿道外括约肌（EUS）和肛门外括约肌（EAS）的操作静息肌节长度（L），并使用模拟分娩损伤（SBI）阴道扩张模型确定 EUS 和 EAS 与分娩相关损伤的机制。
将 3 个月大的 Sprague-Dawley 对照组和损伤组的 EUS 和 EAS 固定在原位，收获并进行微解剖以测量 L 并评估超微结构。分别使用漏点压（LPP）和肛门直肠测压（ARM）在 SBI 前、立即和 4 周后测定 EUS 和 EAS 功能。使用单样本学生 t 检验将操作 L 与特定物种的最佳 L 进行比较。使用重复测量单向方差分析比较组间和时间点的数据（均值±标准差），然后进行 Tukey 事后两两比较，显著性水平设为 0.05。
两个括约肌的操作静息 L（EUS：2.09±0.07µm，EAS：2.02±0.03µm）均明显短于大鼠的最佳 L（2.4µm）。与对照组相比，SBI 对 EUS 和 EAS 施加的应变导致肌节明显伸长和破坏（EUS：3.09±0.11µm，EAS：3.37±0.09µm）。与结构变化平行，LPP 和 ARM 测量值在 SBI 后立即（LPP：21.5±1.0cmH₂O，ARM：5.1±2.31cmH₂O）和 4 周（LPP：27.7±1.3cmH₂O，ARM：2.5±1.0cmH₂O）明显低于基线（LPP：43.4±8.5cmH₂O，ARM：8.2±2.0cmH₂O）；P<0.05。
与人类类似，大鼠 EUS 和 EAS 的短静息 L 有利于其括约肌功能。这些肌肉在分娩过程中受到的损伤会导致肌节过度伸长、肌纤维破坏和括约肌长期功能障碍。
