Effects of Neuromodulation on Bladder Functions in Rats with Detrusor-Sphincter Dyssynergia
Date Issued
2015
Date
2015
Author(s)
Lin, Yin-Tsong
Abstract
Bladder dysfunction often occurs in spinal cord injury (SCI) or diabetes mellitus. Few studies have explored the feasibility of pudendal neuromodulation in regulating bladder functions. Two aims of the present study: the first was electrical activation of the pudendal sensory branch in improving voiding functions in rats 6 weeks after a SCI and the second was chronic microstimulation of the pudendal sensory branch in improving the voiding functions in diabetic rats for 3 or 6 weeks. To assess the effects of electrical stimulation (ES) on bladder and urethral functions, there were two urodynamic measurements for SCI rats: simultaneous recordings of the intravesical pressure (IVP) during continuous isotonic transvesical infusion (isotonic IVP) and external urethral sphincter-electromyography (EUS-EMG), and simultaneous recordings of transvesical pressure under isovolumetric conditions (isovolumetric IVP) and urethral perfusion pressure (UPP). And for electrical microstimulation diabetic rats, the effects of on bladder and urethral functions were assessed by simultaneous recordings of the IVP during continuous isotonic IVP, EUS-EMG, and urine flow rate (UFR). For SCI rats, our results revealed abnormal cystometric measurements, including increases in the volume threshold (VT), contraction amplitude (CA), and residual volume as well as decreased voided volume, which indicated voiding dysfunction in rats 6 weeks after an SCI. The voiding efficiency (VE) decreased to 13% after the SCI, which increased to 22%~34% after applying pudendal afferent stimulation. In addition, pudendal stimulation significantly increased the EUS burst period (EUS-BP) and the difference between the UPP and the high-frequency oscillation (HFO) baselines, and changed the time offset between bladder and EUS activities. On the other hand, our results revealed abnormal cystometric measurements, including increases in the VT, CA, and contraction duration, which indicated voiding dysfunction in diabetic rats of 3 or 6 weeks. The VE decreased to 18% at diabetic rats with sham ES of 6 weeks, which increased to ~50% after applying chronic pudendal microstimulation of 6 weeks. In addition, chronic pudendal microstimulation significantly changed the EUS-BP, mean of UFR and flow duration. All of these findings suggest that pudendal afferent stimulation improved the VE by prolonging the micturition interval, decreasing the urethral resistance, and recovering the detrusor-sphincter dyssynergia during the voiding phase in SCI rats and chronic pudendal microstimulation improved the VE by increasing mean of UFR, and reducing diabetic neuropathy on pudendal nerve in diabetic rats. This study demonstrates the feasibility of pudendal neuromodulation in rats with chronic SCI or chronic diabetes. These results could be as the base for developing an advanced neural prosthesis to restore bladder function in clinical settings.
Subjects
neuromodulation
detrusor-sphincter dyssynergia
bladder function
pudendal nerve
SDGs
Type
thesis
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