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Spinal Micturition Reflex Mediated by Afferents in the Deep Perineal Nerve

¹Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio; and ²Department of Biomedical Engineering, Duke University, Durham, North Carolina

Submitted 20 September 2004; accepted in final form 12 December 2004

Reflexes mediated by urethral sensory pathways are integral to urinary function. This study investigated the changes in bladder pressure and urethral sphincter activity resulting from electrical stimulation of afferents in the deep perineal nerve (DP), which innervates the urethra and surrounding muscles, before and after acute spinal cord transection (SCT) in cats anesthetized with -chloralose monitored by blood pressure and heart rate. DP stimulation elicited bladder contractions before and after SCT but only if the bladder contained a sufficient volume of fluid (78% of the volume needed to cause distention-evoked reflex contractions). The volume dependency was mediated by a neuronal mechanism in the lumbosacral spinal cord and was not attributable to length-tension properties of the detrusor muscle. Stimulation at 2–40 Hz initiated bladder contractions, but 20–40 Hz was more effective than lower frequencies in evoking and sustaining bladder contractions for the duration of the stimulus train. Decreases in urethral sphincter activity occurred during sustained bladder contractions evoked by 20- to 40-Hz stimulation before and within 16 h after SCT. After SCT, average bladder pressure increases evoked by DP stimulation were smaller than those evoked before SCT, but in some animals, bladder pressures elicited by DP stimulation continued to increase as time after SCT increased and reached pretransection amplitudes at 8–16 h posttransection. These data confirm the presence of a spinal circuit that can mediate coordinated bladder–sphincter responses and show that afferents from the DP can activate this circuit under appropriate conditions.

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