scholarly journals Electrical stimulation of the pudendal nerve promotes neuroregeneration and functional recovery from stress urinary incontinence in a rat model

2018 ◽  
Vol 315 (6) ◽  
pp. F1555-F1564 ◽  
Author(s):  
Hai-Hong Jiang ◽  
Qi-Xiang Song ◽  
Bradley C. Gill ◽  
Brian M. Balog ◽  
Raul Juarez ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Stress Urinary Incontinence ◽  
Rat Model ◽  
Pudendal Nerve ◽  
External Urethral Sphincter ◽  
Sham Stimulation ◽  
Point Pressure ◽  
Separate Cohort ◽  
Stimulation Of

The pudendal nerve can be injured during vaginal delivery of children, and slowed pudendal nerve regeneration has been correlated with development of stress urinary incontinence (SUI). Simultaneous injury to the pudendal nerve and its target muscle, the external urethral sphincter (EUS), during delivery likely leads to slowed neuroregeneration. The goal of this study was to determine if repeat electrical stimulation of the pudendal nerve improves SUI recovery and promotes neuroregeneration in a dual muscle and nerve injury rat model of SUI. Rats received electrical stimulation or sham stimulation of the pudendal nerve twice weekly for up to 2 wk after injury. A separate cohort of rats received sham injury and sham stimulation. Expression of brain-derived neurotrophic factor (BDNF) and βII-tubulin expression in Onuf’s nucleus were measured 2, 7, and 14 days after injury. Urodynamics, leak point pressure (LPP), and EUS electromyography (EMG) were recorded 14 days after injury. Electrical stimulation significantly increased expression of BDNF at all time points and βII-tubulin 1 and 2 wk after injury. Two weeks after injury, LPP and EUS EMG during voiding and LPP testing were significantly decreased compared with sham-injured animals. Electrical stimulation significantly increased EUS activity during voiding, although LPP did not fully recover. Repeat pudendal nerve stimulation promotes neuromuscular continence mechanism recovery possibly via a neuroregenerative response through BDNF upregulation in the pudendal motoneurons in this model of SUI. Electrical stimulation of the pudendal nerve may therefore improve recovery after childbirth and ameliorate symptoms of SUI by promoting neuroregeneration after injury.

scholarly journals Daily bilateral pudendal nerve electrical stimulation improves recovery from stress urinary incontinence

2019 ◽  
Vol 9 (4) ◽  
pp. 20190020 ◽  
Author(s):  
Kangli Deng ◽  
Brian M. Balog ◽  
Dan Li Lin ◽  
Brett Hanzlicek ◽  
Qi-Xiang Song ◽  
...  
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Stress Urinary Incontinence ◽  
Pudendal Nerve ◽  
Sprague Dawley ◽  
External Urethral Sphincter ◽  
Bdnf Expression ◽  
Nerve Crush ◽  
Sprague Dawley Rats ◽  
Point Pressure

Stress urinary incontinence (SUI) in women is strongly associated with childbirth which injures the pudendal nerve (PN) and the external urethral sphincter (EUS) during delivery. Electrical stimulation (ES) can increase brain-derived neurotrophic factor (BDNF) expression in injured neurons, activate Schwann cells and promote neuroregeneration after nerve injury. The aim of this study was to determine if more frequent ES would increase recovery from SUI in a rat model. Forty female Sprague–Dawley rats underwent either sham injury or pudendal nerve crush (PNC) and vaginal distention (VD) to establish SUI. Immediately after injury, electrodes were implanted at the pudendal nerve bilaterally. Each injured animal underwent sham ES, twice per week ES (2/week), or daily ES of 1 h duration for two weeks. Urethral and nerve function were assessed with leak point pressure (LPP), EUS electromyography and pudendal nerve sensory branch potential (PNSBP) recordings two weeks after injury. LPP was significantly increased after daily ES compared to 2/week ES. EUS neuromuscular junction innervation was decreased after injury with sham ES, but improved after 2/week or daily ES. This study demonstrates that daily bilateral ES to the pudendal nerve can accelerate recovery from SUI. Daily ES improved urethral function more than 2/week ES.

Bone marrow mesenchymal stromal cell therapy for external urethral sphincter restoration in a rat model of stress urinary incontinence

2010 ◽  
Vol 30 (3) ◽  
pp. 447-455 ◽  
Author(s):  
Jacques Corcos ◽  
Oleg Loutochin ◽  
Lysanne Campeau ◽  
Nicoletta Eliopoulos ◽  
Manaf Bouchentouf ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Urinary Incontinence ◽  
Stress Urinary Incontinence ◽  
Cell Therapy ◽  
Rat Model ◽  
Mesenchymal Stromal Cell ◽  
Stromal Cell ◽  
Urethral Sphincter ◽  
External Urethral Sphincter

Involvement of reflex urethral closure mechanisms in urethral resistance under momentary stress condition induced by electrical stimulation of rat abdomen

2007 ◽  
Vol 293 (3) ◽  
pp. F920-F926 ◽  
Author(s):  
Izumi Kamo ◽  
Tadatoshi Hashimoto
Keyword(s):  
Urinary Incontinence ◽  
Electrical Stimulation ◽  
Abdominal Pressure ◽  
Intravesical Pressure ◽  
Leak Point Pressure ◽  
Pelvic Nerves ◽  
Urethral Closure ◽  
Urethral Resistance ◽  
Point Pressure ◽  
Stimulation Of

A novel method for evaluating the urethral resistance during abrupt elevation of abdominal pressure was developed in spinalized female rats under urethane anesthesia. Electrical stimulation of abdominal muscles for 1 s induced increases in both the intra-abdominal and the intravesical pressure in a stimulus-dependent manner, and the bladder response was almost lost when the abdomen was opened. The lowest intravesical pressure during electrical stimulation that induced fluid leakage from the urethral orifice (leak point pressure) and the maximal intravesical pressure without urine leakage below the leak point pressure were evaluated as the indexes of urethral resistance. Lower urethral resistance was obtained in the rats whose pelvic nerves or somatic nerves containing pudendal nerves and nerves to iliococcygeus/pubococcygeus muscles were transected bilaterally. In contrast, transection of bilateral hypogastric nerves showed smaller effects. Duloxetine, a drug for stress urinary incontinence, enlarged the reflex urethral closing contractions that were induced by an increase in intravesical pressure and measured using a microtip transducer catheter in the middle urethra. This drug also increased the urethral resistance (leak point pressure), whereas it did not show any effect in the rats whose pelvic nerves were bilaterally transected, showing that the augmentation of the reflex urethral closure by the drug resulted in the elevation of the urethral resistance. From these findings, it was concluded that during momentary elevation of abdominal pressure, the reflex urethral closure mechanisms via bladder-spinal cord-urethral sphincter and pelvic floor muscles greatly contribute to the increase in the urethral resistance to prevent the urinary incontinence.

scholarly journals Effect of a 5-HT1A receptor agonist (8-OH-DPAT) on external urethral sphincter activity in a rat model of pudendal nerve injury

2011 ◽  
Vol 301 (1) ◽  
pp. R225-R235 ◽  
Author(s):  
Shih-Ching Chen ◽  
Chen-Li Cheng ◽  
Wen-Jia Fan ◽  
Jia-Jin Jason Chen ◽  
Chien-Hung Lai ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Rat Model ◽  
Receptor Agonist ◽  
Pudendal Nerve ◽  
Perfusion Pressure ◽  
Urethral Sphincter ◽  
Leak Point Pressure ◽  
External Urethral Sphincter ◽  
Point Pressure ◽  
Pudendal Nerve Injury

Although serotonergic agents have been used to treat patients with stress urinary incontinence, the characteristics of the external urethral sphincter (EUS) activity activated by 5-HT receptors have not been extensively studied. This study examined the effects of the 5-HT1A receptor agonist, 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT), on the EUS-electromyography and resistance of the urethra in a rat model with bilateral pudendal nerve injury (BPNI). Two measurements were utilized to assess the effects of the drug on bladder and urethral functions: the simultaneous recordings of transvesical pressure under isovolumetric conditions [isovolumetric intravesical pressure (IVP)] and urethral perfusion pressure, and the simultaneous recordings of IVP during continuously isotonic transvesical infusion with an open urethra (isotonic IVP) and EUS-electromyography. This study also evaluated the urethral continence using leak point pressure testing. The urethral perfusion pressure and leak point pressure measurements of BPNI rats reveal that 8-OH-DPAT significantly increased urethral resistance during the bladder storage phase, yet decreased resistance during the voiding phase. The entire EUS burst period was significantly prolonged, within which the average silent period increased and the frequency of burst discharges decreased. 8-OH-DPAT also improved the voiding efficiency, as evidenced by the detection of decreases in the contraction amplitude and residual volume, with increases in contraction duration and voided volume. These findings suggest that 8-OH-DPAT not only improved continence function, but also elevated the voiding function in a BPNI rat model.

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