Introduction and hypothesis: This study aims to test the hypothesis that a urethra-to-bladder inhibitory pathway exists through which periurethral neuromuscular electrical stimulation (NMES) inhibits overactive bladder contractions in rats. Methods: Bladder overactivity was induced in 22 female Sprague Dawley rats by injection of ketamine/xylazine/acepromizine (K/X/A). A bipolar electrode was placed surgically in the periurethral region to deliver NMES. Intravesical pressure, bladder inter-contraction interval (ICI) and voided volume (VV) were monitored while the bladder was continuously infused with saline. Results: K/X/A induced more frequent bladder contractions (ICI=48.6±20.1 s, before cutting the pubo-symphasis) compared to a 10-min ICI induced by urethane. NMES significantly increased ICI (63.1±31.3 s before vs. 97.2± 42.9 s after NMES, p<0.001) and VV (0.063=0.041 ml before vs. 0.088=0.044 ml after NMES, p<0.02). Conclusions: Injection of K/X/A may potentially be used as a model of bladder overactivity. NMES inhibits bladder contractions in rats with bladder overactivity, which supports the existence of a urethra-to-bladder inhibitory pathway.
Bibliographical noteFunding Information:
Acknowledgment The authors would like to thank Angela J. Forrest and Kyle A Eidsness for assistance in animal experiments and experimental data analysis. This work was supported in part by an unrestricted grant from American Medical Systems and by funding from the Institute for Engineering in Medicine and the Supercomputing Institute at the University of Minnesota.
- Bladder overactivity
- Intravesical pressure
- Periurethral neuromuscular electrical stimulation
- Urinary incontinence
- Voiding dysfunction