Bladder Instability. is the Primary Defect in the Urethra?

Hindmarsh, Jon; Gosling, P. T.; Deane, Adam M

doi:10.1111/j.1464-410x.1983.tb03397.x

Cited by 67 publications

(32 citation statements)

References 5 publications

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“…If the balance between them is lost an involuntary opening of the urethra might occur. The urethral pressure fall that takes place immediately before the detrusor contraction in normal micturition is mimicked in overactive conditions [Hindmarsh et al, 1983;Petros and Ulmsten, 1993;Wise et al, 1993]. Findings in a recent study from our laboratory support an active role also for the bladder outlet and the urethra in the context of over activity.…”

Section: Introductionsupporting

confidence: 52%

Abnormal urethral motor function is common in female stress, mixed, and urge incontinence

Mattiasson

Teleman

2006

Neurourology and Urodynamics

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Women with stress, urge, and mixed urinary incontinence seem to have a primary neuromuscular disorder in the urethra, which presents itself as an overactive opening mechanism with a urethral pressure fall instead of a pressure increase on provocation during the filling phase of the bladder, and during bladder emptying a more efficient opening of the bladder outlet than in normal women. We suggest that one and the same pathophysiological mechanism participates in female stress, urge, and mixed incontinence.

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Section: Introductionsupporting

confidence: 52%

Abnormal urethral motor function is common in female stress, mixed, and urge incontinence

Mattiasson

Teleman

2006

Neurourology and Urodynamics

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“…Through the urethral detrusor facilitative reflex, an open bladder neck might induce unstable detrusor contraction or urge sensation during the straining condition. 25 If the bladder neck can be closed concomitantly during the pubovaginal sling procedure, the postoperative urgency or urge incontinence might disappear, as observed previously in patients with mixed incontinence who underwent colposuspension. 26 In some women with a nonfunctioning urethra and an acontractile detrusor, the sling cannot be tied very tightly, and the position of the bladder neck has to be elevated to a certain degree.…”

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confidence: 78%

Sonographic evaluation of anatomic results after the pubovaginal sling procedure for stress urinary incontinence.

Kuo

2001

J of Ultrasound Medicine

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Objective. To investigate the anatomic changes after the pubovaginal sling procedure in women with stress urinary incontinence by transrectal sonography. Methods. This study enrolled 56 women with varying types of stress urinary incontinence who were treated with the pubovaginal sling procedure using self-fashioned polypropylene mesh. The suburethral sling was fixed without tension and was placed at the position between the bladder neck and the proximal urethra. The patients were investigated preoperatively and postoperatively by transrectal sonography of the bladder and urethra. Results. At a median follow-up of 24 months (range, 6-39 months), 48 patients (85.7%) were cured, 6 (10.7%) had improved, and 2 (3.6%) had treatment failures. Transrectal sonography revealed a wellsuspended bladder neck and proximal urethra in all patients who were cured. As measured by changes of the axis of the pubovesical ligament, the position of the bladder neck was elevated by a mean of 29.6 ± 21.5°in the resting condition and 47.4 ± 27.7°in the straining condition. An incompetent bladder neck and proximal urethra were noted in 8 patients who had stress urinary incontinence after surgery. The incidence of opening of the bladder neck was 84.6% in 13 patients with de novo urgency or urge incontinence, whereas only 2 (4.7%) of 43 patients who did not have postoperative urgency had opening of the neck (P = .000). Conclusion. Transrectal sonography provides useful information about anatomic changes after the pubovaginal sling procedure. Bladder neck incompetence after surgery was closely related to postoperative urgency or urge incontinence.

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“…It has been suggested that unstable detrusor contractions may be initiated from the bladder outlet region rather than from the detrusor itself [32,51]. Morphological changes, e.g., those seen in outflow obstruction caused by benign prostatic hyperplasia, are associated with unstable bladder contractions in 50%-70% of cases [53].…”

Section: Afferent Activity and "Unstable" Bladder Contractionsmentioning

confidence: 99%

Nitric oxide synthase and nitric oxide-mediated effects in lower urinary tract smooth muscles

Andersson

Persson

1994

World J Urol

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In the lower urinary tract smooth muscles, both excitatory and inhibitory non-adrenergic, non-cholinergic (NANC) nerves and neurotransmission can be demonstrated. An inhibitory, relaxation-mediating system may serve not only the detrusor, the trigone, and the bladder neck/urethra, but may also be of importance for their integrated function. Available data suggest that nitric oxide synthase (NOS) is localized in nerve fibres of the lower urinary tract, preferably in the outflow region, and evidence has accumulated that L-arginine-derived nitric oxide (NO) is responsible for the main part of the inhibitory NANC response. Coinciding localization of NOS positive nerves with nerves expressing acetylcholine esterase, vasoactive intestinal peptide, and neuropeptide Y, suggests that NO may have a role both as a directly acting transmitter and as a modulator of efferent neurotransmission. In addition, NO may be involved in afferent neurotransmission. Theoretically, NO released from nerves in the detrusor, could be one factor keeping the bladder relaxed during filling. However, the detrusor has a low sensitivity to NO and agents acting via cyclic GMR which makes it less likely that NO has a role as a relaxant neurotransmitter. This does not exclude that NO may modulate the effects of other transmitters, or that it has an afferent function. NO effectively relaxes isolated smooth muscle preparations from the outflow region, suggesting that it may be involved in the decrease in intraurethral pressure associated with normal micturition, and with the excessive urethral pressure variations ("unstable urethra"), which may be associated with certain voiding disturbances in women. The L-arginine/NO system may also control afferent activity in the outlet region, where lack of NO may lower the threshold for afferent firing leading to bladder instability. Another possible site where the L-arginine/NO pathway can have a functional role is in the urethral lamina propria. Here, NO-mediated relaxation may influence the "inner urethral softness", and thereby the sealing function of the urethral mucosa. However, it should be stressed that the functional importance of the L-arginine/NO system in the central and peripheral pathways controlling micturition remains to be established. Correspondence to: K.-E. Andersson, M.D., Ph.D., Fax: 46 (46) 111987Nonadrenergic, noncholinergic (NANC) nerves and neurotransmission can be demonstrated in lower urinary tract smooth muscles [4,35] as well as in smooth muscles from, e.g., the gastrointestinal tract, the airways, and the genital region [4,17]. In the lower urinary tract, both excitatory and inhibitory NANC-mediated responses have been described [3,4,7,42]. Even if the occurrence of a NANC-mediated contraction in the human detrusor has been questioned, there seems to be a purinergic contractile component of the response to electrical stimulation of nerves [4,35]. Such a component, which seems to be of limited significance in the normal bladder, may be important in, e.g., interstitial cystitis [62]. ...

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Bladder Instability. is the Primary Defect in the Urethra?

Cited by 67 publications

References 5 publications

Abnormal urethral motor function is common in female stress, mixed, and urge incontinence

Abnormal urethral motor function is common in female stress, mixed, and urge incontinence

Sonographic evaluation of anatomic results after the pubovaginal sling procedure for stress urinary incontinence.

Nitric oxide synthase and nitric oxide-mediated effects in lower urinary tract smooth muscles

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