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PubMed2002

Overactive bladder--pharmacological aspects.

The micturition reflex can be initiated by contraction or distension of detrusor smooth muscle cells, or by signals from the urothelium. It has been shown that bladder distension causes release of ATP from the urothelium, and that ATP can activate P2X3 receptors on suburothelial afferent nerve terminals to evoke a neural discharge. However, most probably the activation of afferent fibres during bladder filling involves not only ATP, but a cascade of inhibitory and stimulatory transmitters/mediators. These mechanisms may be targets for future drugs. Both in the normal and functionally disturbed bladder, muscarinic receptor stimulation produces the main part of detrusor contraction, but evidence is accumulating that in disease states, such as neurogenic bladders, outflow obstruction, idiopathic detrusor instability, interstitial cystitis, and also in the ageing bladder, a non-cholinergic activation via purinergic receptors may occur. If this component of activation is responsible not only for part of the bladder contractions, but also for the symptoms of the overactive bladder, it should be considered an important target for therapeutic interventions. Drags blocking different P2X receptor subtypes, or counteracting bladder contraction via other mechanisms, e.g. beta3-adrenoceptor stimulation, may be developed for treatment of the overactive bladder.

Adenosine Triphosphate↗
PubMed1994

Urodynamic characteristics of women with complete posthysterectomy vaginal vault prolapse.

OBJECTIVES: To review the symptoms and lower urinary tract function in women with posthysterectomy vaginal vault prolapse. METHODS: A retrospective review was carried out of the urodynamic records of 19 women with posthysterectomy vaginal vault prolapse who had been evaluated in the Bladder Function Laboratory of the Department of Obstetrics and Gynecology at Duke University Medical Center. RESULTS: A full urodynamic evaluation was carried out on 19 women who had had a hysterectomy and who had subsequently experienced complete prolapse of the vaginal vault. Vaginal eversion produced massive distortion of the lower urinary tract and was associated with complex symptoms. Among the cystometric findings in these patients was an early average first desire to void (94 mL) and a reduced average cystometric capacity (370 mL). Symptoms of voiding difficulty were common. During noninstrumented uroflowmetry, the average peak and mean flow rates were reduced in these women (16.5 mL/s and 8.1 mL/s, respectively), suggestive of functional obstruction of the outlet due to the prolapse. Pressure-flow voiding studies showed a reduced peak flow rate (11 mL/s) with an increased detrusor pressure at peak flow (50 cm H2O), also indicative of functional obstruction. All women underwent urethrocystoscopy, and no patient had a urethral stricture or urethral stenosis. Although symptoms of urgency (79%) and urge incontinence (63%) were common, detrusor instability was confirmed by urodynamic studies in only 3 women (16%), suggesting that urge-related symptoms in these women may often be due to anatomic distortion of the lower urinary tract rather than to detrusor overactivity. "Genuine" stress incontinence was documented in only 2 women (11%) during cystometry; however, when these patients were examined with full bladders with their prolapses reduced and returned to a normal anatomic position with a single-bladed speculum, the physical sign of stress incontinence was demonstrated in all 9 women (47%) who had a complaint of stress incontinence. This suggests that massive vaginal prolapse may mask an incompetent continence mechanism, which may then be revealed after surgical repair of the prolapse. CONCLUSIONS: Women with posthysterectomy vaginal vault prolapse present complicated reconstructive problems for the pelvic surgeon. The same pathophysiological process may produce both voiding dysfunction and stress incontinence. These patients should be evaluated carefully before surgical repair is undertaken. Stress incontinence may not be demonstrated in these patients unless they are examined with a full bladder with their prolapse carefully reduced to a normal anatomic position. Women who demonstrate stress incontinence with the vaginal prolapse reduced and the urethra supported normally should be suspected of having "type III" incontinence (demonstrable stress incontinence in the presence of normal urethral support). Women with these findings may require a suburethral sling procedure if they are to remain continent after correction of posthysterectomy vaginal vault eversion.

Adult↗
PubMed1999

Effects of nifedipine on bladder overactivity in rats with cerebral infarction.

PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.

Animals↗
PubMed2004

The association of diet and other lifestyle factors with the onset of overactive bladder: a longitudinal study in men.

OBJECTIVE: To investigate associations between diet and non-dietary lifestyle factors and the onset of overactive bladder (OAB) in men. SUBJECTS: Random sample of community-dwelling men aged 40 years plus. DESIGN AND METHODS: Baseline data on urinary symptoms and diet were collected from 5454 men using a postal questionnaire and a food-frequency questionnaire. Follow-up data on urinary symptoms were collected from 4887 men in a postal survey one year later. Logistic regression analysis was used to investigate diet and lifestyle factors associated with onset of OAB in the men without OAB at baseline. RESULTS: There was a highly significant negative association between beer intake at baseline and subsequent OAB onset (P=0.001), with reduced risk at all levels of intake compared with those who seldom/never drank beer. Adjustment for total alcohol intake (g ethanol day(-1)) reduced the significance of the association (P=0.02). None of the food groups studied was associated with OAB onset, with the possible exception of potatoes (P=0.05), which showed an increased risk of onset at the highest level of consumption. Physical activity, smoking and obesity were not significantly associated. CONCLUSIONS: While most diet and lifestyle factors were not associated with OAB onset, the evidence from this prospective longitudinal study suggests that beer may have a protective role in the development of OAB. This could be due to a non-alcoholic ingredient as well as the alcohol content.

Adult↗
PubMed2006

[Biofeedback therapy for urinary incontinence in children].

INTRODUCTION: We evaluated the efficacy of biofeedback (BFB) therapy in childrens with functional urinary incontinence refractory to conventional treatment. MATERIALS AND METHODS: 34 patients where included (26 girls and 8 boys). They received BFB therapy during the last year for daytime urinary incontinence. 27 patients had urge syndrome with detrusor overactivity, 3 presented giggle incontinence and 4 patients had dysfunctinal voiding. Mean age was 8,4 years. All cases were refractory to bladder training and/or anticholinergics, or recidived after supression. The BFB therapy was carried out with surface electrodes during bladder filling (29 patients) and during voiding (4 patients). One received both therapies. RESULTS: 15 patients (44%) achieved total continence (daytime and nightime) and 7 (20,5%) responded partially. 9 Patients (26%) didn't obtain any benefit and 4 were losed. CONCLUSIONS: In children with functional urinary incontinence pelvic floor muscles training with biofeedback is a simple and effective method. It should be used associated to other therapies, when these fails or repeats after an initial success.

Biofeedback, Psychology↗
PubMed1998

Micturitional disturbance in patients with chronic inflammatory demyelinating polyneuropathy.

Eight of 32 patients (25%) with chronic inflammatory demyelinating polyneuropathy (CIDP) had micturitional disturbance, which consisted of voiding difficulty (n = 4), urgency (n = 4), or urgency incontinence (n = 1). Urodynamic studies on four symptomatic patients showed disturbed bladder sensation in two, bladder areflexia in one, and neurogenic changes of the external sphincter in one, indicative of peripheral parasympathetic and somatic nerve dysfunctions. Cystometry also showed detrusor overactivity in two patients but no evidence of CNS involvement, evidence that bladder overactivity occurs by probable pelvic nerve irritation.

Adolescent↗
PubMed2006

Upper and lower urinary tract evaluation of 104 patients with myelomeningocele without adequate urological management.

To evaluate the upper and lower urinary tract and revise the urodynamic parameters on myelomeningocele patients without adequate urological management. 104 myelomeningocele patients without previous adequate urological management were assessed by clinical, urodynamic and imaging evaluation. The urodynamic.data were correlated with the status of the upper urinary tract (UUT). Thirty patients presented with vesico-ureteral reflux. Six patients presented signs of UUT damage without reflux. The cystometry showed detrusor overactivity (DO), poor compliance, increased bladder capacity and normal cystometry in 48, 49, 2 and 1% of the patients, respectively. Detrusor leak point pressure (DLPP) over 40 cm H(2)O was associated with UUT damage. Patients with decrease on functional bladder capacity (FBC) or= 40 cm H(2)O and decrease in FBC <or= 33% are associated with greater UUT damage. DO and poor compliance are predominant and pose similar risk of UUT damage.

Adolescent↗
PubMed2000

Electrical stimulation in overactive bladder.

Electrical stimulation is an effective and well-tolerated treatment for overactive bladder. Initial work in animals indicated the potential of this treatment, and early clinical experience in Europe further supported its likely efficacy. Although the mechanism of action of electrical stimulation remains unproven in humans, it is believed to be a neuromodulating therapy which affects the neural signaling that controls continence. There is also strong evidence that electrical stimulation affects striated muscle. The therapy can cause hypertrophy of skeletal muscle fibers, possibly by the recruitment of faster-conducting motor units, which would not normally be recruited during voluntary efforts. In addition, electrical stimulation can alter the expression of myosin isoforms, favoring a conversion to type I muscle. Despite our incomplete understanding of the mechanism of action of electrical stimulation, clinical devices have been developed quickly. Case series have been reported throughout Europe. These were followed by controlled clinical trials in the United States. There is good evidence that the use of vaginal electrical stimulators can reduce the occurrence of symptoms of overactive bladder in about half of the patients treated. Multiple uses of nonimplanted stimulation, including thigh stimulation, anal stimulation, and direct pelvic muscle stimulation, have been reported. In these trials, it is common for objective findings to be poorly correlated with subjective reports of improvements or cure. Patients frequently report that the urge-to-leak time improves, but this is difficult to measure objectively. The use of nonimplanted devices is effective and well tolerated, and should precede the use of implanted devices. A direct comparison with other effective methods of treatment for overactive bladder is warranted.

Adult↗
PubMed1996

[Intravesical oxybutynin hydrochloride in the treatment of urge incontinence in the elderly].

PURPOSE: This study was carried out to determine the effectiveness of intravesical oxybutynin hydrochloride on urinary urge incontinence in elderly people. METHODS: The subjects consisted of 13 patients with an average age of 75 years who demonstrated uninhibited detrusor contraction on cystometrogram. The trial protocol consisted of a pretreatment cystometrogram followed by the intravesical administration of 10 ml solution containing 5 mg oxybutynin hydrochloride (pH 5.85). The urodynamic studies were repeated one hour later. RESULTS: The mean bladder capacity before and after one hour of intravesical oxybutynin hydrochloride was 161 +/- 62 ml and 196 +/- 71 ml (mean +/- 1 S.D., n.s.). The rate of improvement was 15.4% (2 cases) in all 13 patients. Four patients out of 13 patients continued intravesical administration of the solution twice daily. Urinary incontinence disappeared in two patients and incontinence was markedly decreased in one. In the remaining patient, urinary incontinence did not change because of increased residual urine. Three patients have continued this therapy over one years and no side effects were observed. In these patients, residual urine volume did not increase. CONCLUSION: It is suggested that intravesical oxybutynin hydrochloride is an effective option of therapy for intractable urge incontinence in elderly people, however, the immediate posttreatment cystometrogram was not predictive of the response to intravesical therapy on overactive bladder in the elderly.

Administration, Intravesical↗
PubMed2006

Spinal ERK activation contributes to the regulation of bladder function in spinal cord injured rats.

The extracellular signal-regulated kinase 1 and 2 (ERK) pathway, regulated by phosphorylation on specific amino acids, is emerging as an important signaling cascade in neurones, transducing sensory input into cellular responses. In the mammalian nervous system, the ERK pathway has been found to mediate plasticity events. Particularly, in the spinal cord, ERK play an important role in allodynia and hyperalgesia. Recently, it was demonstrated that ERK activation is upregulated in the spinal cord of rats with chronic bladder inflammation and contributes to bladder overactivity. Thus, in this study we sought to assess the involvement of ERK in micturition reflexes associated to spinal cord injury (SCI) in the rat. Bladder function in chronic SCI rats was altered compared to spinal intact rats. PhosphoERK levels were upregulated in the L6 spinal cord segment, particularly after saline infusion for 2 h. The increase in spinal ERK phosphorylation was specifically restricted to L6 spinal segment. No variation in the levels of total ERK protein was observed. Intrathecal administration of PD98059, a specific inhibitor of ERK phosphorylation, reduced the frequency and amplitude of bladder contractions in SCI animals but not in spinal intact ones. Overall, our results demonstrate increased activation of the ERK pathway in the spinal cord from SCI rats, restricted to spinal segments that receive sensory input arising from the bladder. Since the use of PD98059 reduced the frequency and amplitude of bladder contractions, ERK inhibitors may provide a new therapeutic approach to the treatment of bladder overactivity after spinal injuries.

Animals↗
PubMed1997

Antimuscarinic potency and bladder selectivity of PNU-200577, a major metabolite of tolterodine.

PNU-200577 (labcode DD 01 [(R)-N, N-diisopropyl-3-(2-hydroxy-5-hydroxymethylphenyl)-3-phenylpropanamine ) is a major pharmacologically active metabolite of tolterodine, a new muscarinic receptor antagonist intended for the treatment of an overactive bladder. In vitro, PNU-200577 produced a competitive and concentration-dependent inhibition of carbachol-induced contraction of guinea-pig isolated urinary bladder strips (KB = 0.84 nM; pA2 = 9.14). In vivo, PNU-200577 was significantly more potent at inhibiting acetylcholine-induced urinary bladder contraction than electrically induced salivation in the anaesthetised cat (ID50 15 and 40 nmol.kg-1, respectively; P < 0.01). In radioligand binding studies carried out in homogenates of guinea-pig tissues and Chinese hamster ovary cell lines expressing human muscarinic m1-m5 receptors, PNU-200577 was not selective for any muscarinic receptor subtype. Thus, PNU-200577 is similar to tolterodine in terms of antimuscarinic potency, functional selectivity for the urinary bladder in vivo and absence of selectivity for muscarinic receptor subtypes in vitro. The results of this study clearly indicate that PNU-200577 contributes to the therapeutic action of tolterodine, in view of its high antimuscarinic potency, similar serum concentration and lower degree of protein binding.

Acetylcholine↗