International urogynecology journal · 2026
Low-Intensity Extracorporeal Shock Wave Therapy Restores Passive Urethral Closure Mechanism in Vaginal Distension Rat Model.
СтатьяНазвание и аннотация: Перевод в очереди
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Akimoto Takahiro, Ashikari Asuka, Kurobe Masahiro, Takamatsu Gakuya, Akiyama Yoshiyuki, Kume Haruki, Miyazato Minoru
Аннотация
INTRODUCTION AND HYPOTHESIS: Low-intensity extracorporeal shock wave therapy (LiESWT) is a promising noninvasive therapy for stress urinary incontinence (SUI). We assessed whether LiESWT restores urethral function in a vaginal distension (VD)-induced rat model of SUI, focusing on pelvic floor tissue remodeling and endoplasmic reticulum stress pathway as potential mechanisms.
METHODS: Eighty-one female Sprague-Dawley rats underwent functional and tissue analyses. Sneezing was induced to assess urethral pressure responses. Leak point pressure (LPP) was measured with or without hypogastric and pudendal nerve transections. Tissue remodeling and molecular pathways were assessed using histological and molecular expression analyses.
RESULTS: In VD rats, baseline urethral pressure (9.9 ± 4.3 vs 17.6 ± 3.1 cmH2O) and LPP (27.4 ± 4.7 vs 37.0 ± 7.0 cmH2O) were lower than in normal rats (both p < 0.05). LiESWT restored the baseline urethral pressure (16.3 ± 4.7 cmH2O) and LPP (37.5 ± 4.9 cmH2O) in VD rats (p < 0.05). Notably, LPP enhancement persisted after bilateral hypogastric and pudendal nerve transections. Additionally, LiESWT tended to reduce VD-induced vaginal smooth muscle fibrosis histologically, whereas collagen type I alpha and elastin mRNA expression remained elevated in both groups. Western blotting revealed no sustained activation of protein kinase R-like endoplasmic reticulum kinase (PERK) at 96 h after the final LiESWT.
CONCLUSIONS: LiESWT enhanced urethral function in the VD-induced SUI model by potentially facilitating pelvic floor tissue remodeling, thereby restoring passive urethral closure. The absence of sustained PERK activation in the late phase indicates the safety of LiESWT for SUI.
METHODS: Eighty-one female Sprague-Dawley rats underwent functional and tissue analyses. Sneezing was induced to assess urethral pressure responses. Leak point pressure (LPP) was measured with or without hypogastric and pudendal nerve transections. Tissue remodeling and molecular pathways were assessed using histological and molecular expression analyses.
RESULTS: In VD rats, baseline urethral pressure (9.9 ± 4.3 vs 17.6 ± 3.1 cmH2O) and LPP (27.4 ± 4.7 vs 37.0 ± 7.0 cmH2O) were lower than in normal rats (both p < 0.05). LiESWT restored the baseline urethral pressure (16.3 ± 4.7 cmH2O) and LPP (37.5 ± 4.9 cmH2O) in VD rats (p < 0.05). Notably, LPP enhancement persisted after bilateral hypogastric and pudendal nerve transections. Additionally, LiESWT tended to reduce VD-induced vaginal smooth muscle fibrosis histologically, whereas collagen type I alpha and elastin mRNA expression remained elevated in both groups. Western blotting revealed no sustained activation of protein kinase R-like endoplasmic reticulum kinase (PERK) at 96 h after the final LiESWT.
CONCLUSIONS: LiESWT enhanced urethral function in the VD-induced SUI model by potentially facilitating pelvic floor tissue remodeling, thereby restoring passive urethral closure. The absence of sustained PERK activation in the late phase indicates the safety of LiESWT for SUI.