scholarly journals Nav1.9 regulates bladder capacity in cyclophosphamide‐induced overactive bladder

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Kevin Thorneloe ◽  
Amy M Ritter ◽  
Birgit T Priest ◽  
William J Martin
Keyword(s):  
Overactive Bladder ◽  
Bladder Capacity

scholarly journals Stimulation of the sensory pudendal nerve increases bladder capacity in the rat

2018 ◽  
Vol 314 (4) ◽  
pp. F543-F550 ◽  
Author(s):  
James A. Hokanson ◽  
Christopher L. Langdale ◽  
Arun Sridhar ◽  
Warren M. Grill
Keyword(s):  
Overactive Bladder ◽  
Nerve Stimulation ◽  
Therapeutic Efficacy ◽  
Pudendal Nerve ◽  
Bladder Capacity ◽  
Lower Urinary Tract Dysfunction ◽  
Pudendal Nerve Stimulation ◽  
Female Wistar Rats ◽  
Promising Treatment ◽  
Stimulation Of

Pudendal nerve stimulation is a promising treatment approach for lower urinary tract dysfunction, including symptoms of overactive bladder. Despite some promising clinical studies, there remain many unknowns as to how best to stimulate the pudendal nerve to maximize therapeutic efficacy. We quantified changes in bladder capacity and voiding efficiency during single-fill cystometry in response to electrical stimulation of the sensory branch of the pudendal nerve in urethane-anesthetized female Wistar rats. Increases in bladder capacity were dependent on both stimulation amplitude and rate. Stimulation that produced increases in bladder capacity also led to reductions in voiding efficiency. Also, there was a stimulation carryover effect, and increases in bladder capacity persisted during several nonstimulated trials following stimulated trials. Intravesically administered PGE2 reduced bladder capacity, producing a model of overactive bladder (OAB), and sensory pudendal nerve stimulation again increased bladder capacity but also reduced voiding efficiency. This study serves as a basis for future studies that seek to maximize the therapeutic efficacy of sensory pudendal nerve stimulation for the symptoms of OAB.

Botulinum toxin therapy for nonneurogenic overactive bladder: first experience

2011 ◽  
Vol 18 (3) ◽  
pp. 120-126
Author(s):  
Aušra ČERNIAUSKIENĖ ◽  
Feliksas JANKEVIČIUS
Keyword(s):  
Botulinum Toxin ◽  
Overactive Bladder ◽  
Botulinum Toxin A ◽  
Urine Volume ◽  
Bladder Capacity ◽  
Anticholinergic Drugs ◽  
Detrusor Muscle ◽  
Residual Urine Volume ◽  
Toxin A

The paper presents early experience in the treatment of 20 patients with botulinum toxin injections into the detrusor muscle for the treatment of non-neurogenic overactive bladder (OAB) resistant to anticholinergic drugs. Background. Botulinum toxin, a presynaptic neuromuscular blocking agent, reduces the involuntary bladder contractions that cause urgency, frequency and urge incontinence. We present our early experience with Dysport® injections into the detrusor for the treatment of non–neurogenic overactive bladder (OAB) resistant to anticholinergic drugs. Materials and methods. Using intravenous anaesthesia, 20 patients (18 female and 2 male) with non-neurogenic OAB were injected with botulinum toxin A (Dysport®250 IU diluted in 4 ml normal saline) under cystoscopic visualization in 20 sites in the detrusor muscle, sparing the trigone. The urethral catheter was removed 24 hours after the procedure. Follow-up at 3 and 6 months after the injection included the Urogenital Distress Inventory UDI-6, the Incontinence Impact Questionnaire IIQ-7, clinical parameters and ultrasound measurement of bladder capacity and post-void residual urine volume. Results. All 20 patients completed questionnaires and were examined after 3 and 6 months. At the 3-month follow-up, the median daytime micturation frequency decreased from 10.4 to 4.6 times (p < 0.0001) and at the 6 months follow-up 5 times (p < 0.0001), while nocturia decreased from 4.2 to 1.3 times after 3 months (p < 0.0001) and after 6 months to 2 times (p < 0.0001). Urgency decreased from 6 to 1.5 times after 3 months (p < 0.0001) and to 2 times after 6 months (p < 0.0001), and incontinence decreased from 4.2 times to 1.5 times after 3 months (p < 0.0001) and to 2.1 times after 6 months (p < 0.0001). The median maximum bladder capacity increased from 250 to 420 ml after 3 months (p < 0.0001) and decreased to 350 ml after 6 months (p < 0.0001). The post-void median residual urine volume was 10 ml. Only one patient mentioned a post-operative obstructive voiding difficulty. Eighteen (90%) patients were satisfied with the treatment. In two patients (10%), the amelioration of symptoms lasted for one month only, and later OAB symptoms reappeared. Analysis of the UDI-6 and IIQ-7 questionnaires revealed that botulinum toxin A intradetrusor injection had decreased discomfort for patients and ameliorated their quality of life. Conclusions. Botulinum toxin A injections in the detrusor are effective for the treatment of non-neurogenic OAB. Botulinum toxin A injections are a minimally invasive therapy and offer an alternative treatment for non–neurogenic OAB dysfunction resistant to conservative treatment. The durability of the treatment effect is the objective of the further investigation. Keywords: botulinum toxin, overactive bladder, urinary incontinence

scholarly journals Low Intensity Extracorporeal Shock Wave Therapy as a Potential Treatment for Overactive Bladder Syndrome

Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 540
Author(s):  
Jian-He Lu ◽  
Kuang-Shun Chueh ◽  
Shu-Mien Chuang ◽  
Yi-Hsuan Wu ◽  
Kun-Ling Lin ◽  
...  
Keyword(s):  
Shock Wave ◽  
Overactive Bladder ◽  
Social Activity ◽  
Extracorporeal Shock Wave Therapy ◽  
Bladder Capacity ◽  
Shock Wave Therapy ◽  
Low Intensity ◽  
Extracorporeal Shock Wave ◽  
Voided Volume

Background: The present study attempted to investigate the therapeutic effect and duration of low intensity extracorporeal shock wave therapy (LiESWT) on overactive bladder (OAB) symptoms, including social activity and the quality of life (QoL). Methods: In this prospective, randomized, single-blinded clinical trial, 65 participants with OAB symptom were randomly divided into receive LiESWT (0.25 mJ/mm2, 3000 pulses, 3 pulses/second) once a week for 8 weeks, or an identical sham LiESWT treatment without the energy transmission. We analyzed the difference in overactive bladder symptom score (OABSS) and 3-day urinary diary as the primary end. The secondary endpoint consisted of the change in uroflowmetry, post-voided residual (PVR) urine, and validated standardized questionnaires at the baseline (W0), 4-week (W4) and 8-week (W8) of LiESWT, and 1-month (F1), 3-month (F3) and 6-month (F6) follow-up after LiESWT. Results: 8-week LiESWT could significantly decrease urinary frequency, nocturia, urgency, and PVR volume, but meaningfully increase functional bladder capacity, average voided volume and maximal flow rate (Qmax) as compared with the W0 in the LiESWT group. In addition, the scores calculated from questionnaires were meaningfully reduced at W4, W8, F1, F3, and F6 in the LiESWT group. Conclusions: Our results revealed that the therapeutic efficacy of LiESWT could improve voided volume and ameliorate OAB symptoms, such as urgency, frequency, nocturia, and urinary incontinence, and lasted up to 6 month of follow-up. Moreover, LiESWT treatment brought statistically significant and clinically meaningful improvements in social activity and QoL of patients. These findings suggested that LiESWT could serve as an alternative non-invasive therapy for OAB patients.

scholarly journals OAB without an overactive bladder in the acute prostaglandin E2 rat model

2017 ◽  
Vol 313 (5) ◽  
pp. F1169-F1177 ◽  
Author(s):  
James A. Hokanson ◽  
Christopher L. Langdale ◽  
Arun Sridhar ◽  
Warren M. Grill
Keyword(s):  
Overactive Bladder ◽  
Prostaglandin E2 ◽  
Perfusion Pressure ◽  
Bladder Dysfunction ◽  
Bladder Capacity ◽  
Wistar Rat ◽  
Bladder Compliance ◽  
Urethral Smooth Muscle ◽  
Proximal Urethra ◽  
Promising Avenue

Intravesical prostaglandin E2 (PGE2) was previously used to induce overactive bladder (OAB) symptoms, as it reduces bladder capacity in rats and causes a “strong urgency sensation” in healthy women. However, the mechanism by which this occurs is unclear. To clarify how PGE2 reduces bladder capacity, 100 µM PGE2 was administered intravesically during open, single-fill cystometry with simultaneous measurement of sphincter EMG in the urethane-anesthetized female Wistar rat. PGE2 was also applied to the urethra or bladder selectively by use of a ligature at the bladder neck before (urethra) or during (bladder) closed-outlet, single-fill cystometry. Additional tests of urethral perfusion with PGE2 were made. PGE2 decreased bladder capacity, increased voiding efficiency, and increased sphincter EMG during open cystometry compared with saline controls. The number of nonvoiding contractions did not change with PGE2; however, bladder compliance decreased. During closed-outlet cystometry, PGE2 applied only to the bladder or the urethra did not decrease bladder capacity. Urethral infusion of PGE2 decreased urethral perfusion pressure. Taken together, these results suggest that intravesical PGE2 may decrease bladder capacity by targeting afferents in the proximal urethra. This may occur through urethral relaxation and decreased bladder compliance, both of which may increase activation of proximal urethra afferents from distension of the proximal urethra. This hypothesis stands in contrast to many hypotheses of urgency that focus on bladder dysfunction as the primary cause of OAB symptoms. Targeting the urethra, particularly urethral smooth muscle, may be a promising avenue for the design of drugs and devices to treat OAB.

scholarly journals Stimulation of the pelvic nerve increases bladder capacity in the PGE2 cat model of overactive bladder

2020 ◽  
Vol 318 (6) ◽  
pp. F1357-F1368
Author(s):  
Christopher L. Langdale ◽  
James A. Hokanson ◽  
Philip H. Milliken ◽  
Arun Sridhar ◽  
Warren M. Grill
Keyword(s):  
Overactive Bladder ◽  
Bladder Capacity ◽  
Electromyographic Activity ◽  
External Urethral Sphincter ◽  
Pelvic Nerve ◽  
Stimulation Parameters ◽  
Threshold Amplitude ◽  
Cat Model ◽  
Neurologically Intact ◽  
Stimulation Of

Selective electrical stimulation of the pudendal nerve exhibits promise as a potential therapy for treating overactive bladder (OAB) across species (rats, cats, and humans). More recently, pelvic nerve (PelN) stimulation was demonstrated to improve cystometric bladder capacity in a PGE2 rat model of OAB. However, PelN stimulation in humans or in an animal model that is more closely related to humans has not been explored. Therefore, our objective was to quantify the effects of PGE2 and PelN stimulation in the cat. Acute cystometry experiments were conducted in 14 α-chloralose-anesthetized adult, neurologically intact female cats. Intravesical PGE2 decreased bladder capacity, residual volume, threshold contraction pressure, and mean contraction pressure. PelN stimulation reversed the PGE2-induced decrease in bladder capacity and increased evoked external urethral sphincter electromyographic activity without influencing voiding efficiency. The increases in bladder capacity generated by PelN stimulation were similar in the rat and cat, but the stimulation parameters to achieve this effect differed (threshold amplitude at 10 Hz in the rat vs. twice threshold amplitude at 1 Hz in the cat). These results highlight the potential of PGE2 as a model of OAB and provide further evidence that PelN stimulation is a promising approach for the treatment of OAB symptoms.

scholarly journals Stimulation of the pelvic nerve increases bladder capacity in the prostaglandin E2 rat model of overactive bladder

2017 ◽  
Vol 313 (3) ◽  
pp. F657-F665 ◽  
Author(s):  
Christopher L. Langdale ◽  
James A. Hokanson ◽  
Arun Sridhar ◽  
Warren M. Grill
Keyword(s):  
Urinary Tract ◽  
Overactive Bladder ◽  
Rat Model ◽  
Lower Urinary Tract ◽  
Bladder Capacity ◽  
Pelvic Nerve ◽  
Lower Urinary Tract Function ◽  
Tract Function ◽  
Stimulation Of ◽  
Lower Urinary

Overactive bladder (OAB) syndrome is a highly prevalent condition that may lead to medical complications and decreased quality of life. Emerging therapies focusing on selective electrical stimulation of peripheral nerves associated with lower urinary tract function may provide improved efficacy and reduced side effects compared with sacral neuromodulation for the treatment of OAB symptoms. Prior studies investigating the effects of pelvic nerve (PelN) stimulation on lower urinary tract function were focused on promoting bladder contractions, and it is unclear whether selective stimulation of the PelN would be beneficial for the treatment of OAB. Therefore our motivation was to test the hypothesis that PelN stimulation would increase bladder capacity in the prostaglandin E2 (PGE2) rat model of OAB. Cystometry experiments were conducted in 17 urethane-anesthetized female Sprague-Dawley rats. The effects of intravesical PGE2 vs. vehicle and PelN stimulation after intravesical PGE2 on cystometric parameters were quantified. Intravesical infusion of PGE2 resulted in decreased bladder capacity and increased voiding efficiency without a change in bladder contraction area under the curve, maximum contraction pressure, or contraction duration. Bladder capacity was also significantly decreased compared with vehicle (1% ethanol in saline) confirming that the change in bladder capacity was mediated by PGE2. PelN stimulation reversed the PGE2-induced change in bladder capacity and increased the external urethral sphincter electromyogram activity at a specific stimulation condition (amplitude of 1.0 times threshold at 10 Hz). These results confirm that the urodynamic changes reported in conscious rats are also observed under urethane anesthesia and that PelN stimulation is a novel and promising approach for the treatment of the symptoms of OAB.

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