Characterization of bilateral, pudendal nerve-evoked, urethral rhabdosphincter contractions in anesthetized cats

Pudendal (PUD) efferent activity contracts urethral rhabdosphincters to resist urine leakage. This study evaluates the potential for PUD nerve stimulation to provide benefit for urinary incontinence. Acute responses of the urethral rhabdosphincter to modulation of current amplitude, pulse duration (PD), and frequency of stimulation were examined. Urethral pressure was measured using a microtip catheter in chloraloseanesthetized, male cats with or without acute spinalization at T10. Stimulation was applied from an external pulse generator coupled to cuff electrodes placed around left and right PUD nerves in the ischiorectal fossa, central to its branching. Bladder pressure clamp techniques were used for testing effects of stimulation on time and rate of leakage during PUD stimulation. Single pulses (0.1 ms) produced single transient increases in urethral pressure that peaked at 50 ms and diminished to 50% of peak at 90 ms. Threshold current was 88 +/- 30 mu A with maximal responses occurring with 50% increases in current. Peak pressures increased with increasing PDs between 40- 180 mu s. Summation, tetany, peak pressures, and fatigue of responses to increasing stimulation frequencies during 2 min periods of stimulation are described. Stimulation under pressures that are typical during bladder filling or during bladder contractions (30-40 cm H 2 O) prevented leakage up to an hour in some animals, increased the median time to leak from 0.3 min to 56.0 min, and decreased the median rate of leakage from 1.44 ml/min to 0.04 ml/min when leakage did occur in less than hour. During rapid elevations in bladder pressure to simulate a Valsalva-like bladder pressure (120 cm H 2 O), PUD stimulation increased the median time to leak from 9 s to 93 s and decreased the median rate of leakage from 5.5 ml/min to 3.4 ml/min. These results support future studies of bilateral PUD stimulation in a clinically -relevant, animal model of urinary incontinence.