UC San Diego

Aims

To define the operational resting sarcomere length (L_s ) 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.

Methods

EUS and EAS of 3-month-old Sprague-Dawley control and injured rats were fixed in situ, harvested, and microdissected for L_s 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 _s was compared to species-specific optimal L _s 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.

Results

The operational resting L_s of both sphincters (EUS: 2.09 ± 0.07 µm, EAS: 2.02 ± 0.03 µm) was significantly shorter than optimal rat L_s 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 cmH₂ O, ARM: 5.1 ± 2.31 cmH₂ O) and 4 weeks (LPP: 27.7 ± 1.3cmH₂ O, ARM: 2.5 ± 1.0 cmH₂ O) after SBI relative to the baseline (LPP: 43.4 ± 8.5 cmH₂ O, ARM: 8.2 ± 2.0 cmH₂ O); P < 0.05.

Conclusions

Analogous to humans, the short resting L_s 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.