Purpose: Ideal therapy for lower urinary tract dysfunction in patients with spinal cord injury (SCI) should decrease detrusor overactivity, thereby promoting urine storage at low intravesical pressure and promoting efficient voiding at low pressure by decreasing detrusor-sphincter dyssynergia. Here we investigated blockade of various α1-adrenoceptors to determine the subtype that was principally responsible for improving the voiding dysfunction. Materials and Methods: The effects of the intravenous α1A/D-blocker naftopidil, the α1D-blocker BMY 7378, and the α1A-blocker silodosin were evaluated using cystometrography and external urethral sphincter-electromyography (EMG) in decerebrated, unanesthetized female Sprague-Dawley rats with chronic SCI following transection at Th8. Parameters measured included the voided volume, residual volume, voiding efficiency, and burst and silent periods on EMG. Results: Compared to values in decerebrated non-SCI rats, EMG of decerebrated SCI rats revealed more prominent tonic activity, significantly shorter periods of bursting activity, and a reduced ratio of the silent to active period during bursting compared to the values in decerebrated non-SCI rats. Compared to the value before drug administration (control), the voiding efficiency was significantly increased by naftopidil (1 and 3 mg/kg) (p < 0.05 each), and the burst (p < 0.01 and < 0.05, respectively) and silent periods (p < 0.01 each) of EMG were significantly lengthened. BMY 7378 (1 mg/kg) significantly increased voiding efficiency and lengthened the burst periods (each p < 0.05). Silodosin did not affect any parameters. Conclusions: These results suggest that α1D-blockade reduces the urethral resistance associated with detrusor-sphincter dyssynergia, thus improving voiding efficiency in SCI rats.
- external urethral sphincter
- spinal cord injury
- Copyright © 2016, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology