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1

Musci, R., V. Franchini, T. Meroni, O. De Cobelli, B. Frea, G. Bovo, A. M. Milella, E. Rossi, F. Franzetti e U. Pea. "Neurogenic urinary dysfunction in AIDS patients". Urologia Journal 61, n. 2 (aprile 1994): 137–41. http://dx.doi.org/10.1177/039156039406100209.

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Abstract (sommario):
From May 1992 to December 1993 (17 months), 18 patients with AIDS, 15 male and 3 female, age range from 25 to 50, were found to have severe voiding disorders related to neurogenic bladder dysfunction. All patients underwent neurologic, urologic and immunologic evaluation and were staged as AIDS-IVB. The neurological evaluation demonstrated: cryptococcal abscess of the brain in 1 patient, progressive and diffuse leukoencephalopathy in 3 patients, AIDS Dementia Complex in 3 patients and no neurologic abnormalities in 11 patients. The urodynamic tests demonstrated: detrusor areflexia in 5 patients, detrusor hyperreflexia with external sphincter dyssynergia in 5 patients, detrusor hyperreflexia with external sphincter dyssynergia and vesico-ureferai reflux in 1 patient, detrusor hyperreflexia without dyssynergia in 7 patients.
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2

Sakakibara, Ryuji, Ayami Shimizu, Osamu Takahashi, Fuyuki Tateno, Masahiko Kishi, Yosuke Aiba, Hiroyoshi Suzuki, Tatsuya Yamamoto, Chiharu Shibata e Tomonori Yamanishi. "Lower Urinary Tract Function in Familial Spastic Paraplegia". European Neurology 80, n. 3-4 (2018): 121–25. http://dx.doi.org/10.1159/000494030.

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Abstract (sommario):
In order to investigate lower urinary tract function in hereditary spastic paraplegia (HSP), we recruited 12 HSP patients: 8 men, 4 women; mean age, 64.6 years; mean disease duration, 18.9 years; walk without cane, 2, walk with cane, 6, wheelchair bound, 3. We performed urinary symptom questionnaires and a urodynamic testing in all patients. As a result, urinary symptoms were observed in all but 3, including urinary urgency/frequency (also called overactive bladder) in 9 and hesitancy/poor stream in 6. Urodynamic abnormalities included detrusor overactivity during bladder filling in 10, underactive detrusor on voiding in 8 (detrusor hyperactivity with impaired contraction [DHIC] in 5), detrusor-sphincter dyssynergia (DSD) on voiding in 3, and post-void residual in 5. Sphincter electromyography showed neurogenic motor unit potential in 4. In conclusion, we observed high frequency of urinary symptoms in HSP. Urodynamics indicated that the main mechanism is DHIC with/without DSD for their urinary symptom, and sacral cord involvement in some cases. These findings facilitate patients’ care including clean, intermittent catheterization.
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3

Andersson, Karl-Erik, e Anders Arner. "Urinary Bladder Contraction and Relaxation: Physiology and Pathophysiology". Physiological Reviews 84, n. 3 (luglio 2004): 935–86. http://dx.doi.org/10.1152/physrev.00038.2003.

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Abstract (sommario):
The detrusor smooth muscle is the main muscle component of the urinary bladder wall. Its ability to contract over a large length interval and to relax determines the bladder function during filling and micturition. These processes are regulated by several external nervous and hormonal control systems, and the detrusor contains multiple receptors and signaling pathways. Functional changes of the detrusor can be found in several clinically important conditions, e.g., lower urinary tract symptoms (LUTS) and bladder outlet obstruction. The aim of this review is to summarize and synthesize basic information and recent advances in the understanding of the properties of the detrusor smooth muscle, its contractile system, cellular signaling, membrane properties, and cellular receptors. Alterations in these systems in pathological conditions of the bladder wall are described, and some areas for future research are suggested.
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4

Gorbunov, Aleksandr I., Aleksandr N. Murav’ev, Evgenij G. Sokolovich e Petr K. Yablonsky. "Neurogenic urinary disorders in patients with tuberculous spondylitis before and after surgical treatment". Urology reports (St. - Petersburg) 11, n. 1 (27 maggio 2021): 27–32. http://dx.doi.org/10.17816/uroved52482.

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Abstract (sommario):
ABSTRACT: Tuberculosis inflammation of vertebral column (spondylitis) can lead to neurogenic lower urinary tract dysfunction. There is lack of available publications for neurogenic lower urinary tract dysfunction in spinal tuberculosis. OBJECTIVE: To evaluate urodynamic disturbances in spinal tuberculosis before and after surgery for spondylitis. MATERIALS AND METHODS: We observed 19 patients with spinal tuberculosis, who had symptoms of micturitions impairment. 14 patients (73,6%) were male and 5 (26,4%) were female, average age was 43,7 7,9 years (2766). Control evaluation was performed after surgery on day 2128. RESULTS: Before surgery we found detrusor overactivity in 11 (57,9%) patients and 2 of those with detrusor overactivity had detrusor-sphincter dyssynergia. Detrusor hypo-/acontractility was diagnosed in 8 (42,1%). After surgery 5 patients (26,3%) exhibited improvement, in one case urodynamic disturbances were resolved. One patient developed detrusor overactivity and incontinence de novo and one patient had worsening neurological status, loss of sensitivity and acontractile bladder. CONCLUSION: Variable lower urinary tract dysfunction can be diagnosed in spinal tuberculosis. Only 26,3% of patients have improvement after surgery. New conditions or worsening of previous neurogenic lower urinary tract dysfunctions can be observed.
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5

Griffiths, D. J., C. E. Constantinou e R. van Mastrigt. "Urinary bladder function and its control in healthy females". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, n. 2 (1 agosto 1986): R225—R230. http://dx.doi.org/10.1152/ajpregu.1986.251.2.r225.

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Abstract (sommario):
Recordings in eight healthy female volunteers of bladder (detrusor) pressure and flow rate, obtained during bladder filling and during voiding, both through the urethra and through a catheter, demonstrate that a model of bladder function in which the detrusor muscle is considered as completely passive during filling and fully activated during voiding is inadequate. Assessment of the detrusor contraction strength by a new method (described in APPENDIX A) shows that in ideal normal voidings the contraction strength rises to values of 11-24 W/m2 and is sustained or rises slightly until the bladder is empty. During unstable detrusor contractions, which even in these healthy women are observed during bladder filling and also during inhibited voidings through the urethra, the contraction is weaker. During voidings through a catheter the detrusor contraction is weak, variable, and fades away before the bladder is empty. An elementary feedback analysis demonstrates that the effect of the micturition reflex governing detrusor behavior differs according to whether or not voiding is taking place. The reflex does not lead to a simple on-off mechanism but to a more complex behavior that is consistent with the observations and that appears to be important for the understanding of pathological obstructed micturition.
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6

OKAMOTO-KOIZUMI, Takako, Masayuki TAKEDA, Takeshi KOMEYAMA, Akihiko HATANO, Makoto TAMAKI, Takaki MIZUSAWA, Toshiki TSUTSUI et al. "Pharmacological and molecular biological evidence for ETA endothelin receptor subtype mediating mechanical responses in the detrusor smooth muscle of the human urinary bladder". Clinical Science 96, n. 4 (1 aprile 1999): 397–402. http://dx.doi.org/10.1042/cs0960397.

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Abstract (sommario):
The aim of this study was to characterize endothelin receptor subtypes of the detrusor muscle of the human urinary bladder. The receptor subtypes mediating endothelin (ET)-1-induced activity in the human detrusor smooth muscles have been characterized using isometric contraction and reverse transcription–polymerase chain reaction (RT–PCR). ET-1 (a non-selective ET receptor agonist; 10-10 M to 10-6 M) exhibited concentration-dependent contractions in human urinary bladder with a plateau at concentrations above 3×10-7 M. Neither IRL1620 nor sarafotoxin S6c (both ETB-selective agonists; 10-10 M to 10-6 M) elicited contractile activity in the human urinary bladder detrusor smooth muscle. FR139317 (an ETA-selective antagonist; 10-7 M to 10-5 M) produced a marked shift to the right of the ET-1 concentration–response curve in human urinary bladder detrusor smooth muscle (from the Schild plot TpA2 = 7.96; slope = 0.95). In contrast, RES701-1 (an ETB-selective antagonist; 10-7 M to 10-5 M) had no effect on the ET-1 concentration–response curve. RT–PCR revealed positive amplification of ETA receptor mRNA fragment, but not ETB. These results indicate that the ET-1-induced contractile effects of urinary bladder detrusor smooth muscle seem to be mediated mainly by the ETA receptor, not by the ETB receptor.
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7

Heppner, Thomas J., Jeffrey J. Layne, Jessica M. Pearson, Hagop Sarkissian e Mark T. Nelson. "Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, n. 2 (agosto 2011): R351—R362. http://dx.doi.org/10.1152/ajpregu.00656.2010.

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Abstract (sommario):
The muscularis mucosae, a type of smooth muscle located between the urothelium and the urinary bladder detrusor, has been described, although its properties and role in bladder function have not been characterized. Here, using mucosal tissue strips isolated from guinea pig urinary bladders, we identified spontaneous phasic contractions (SPCs) that appear to originate in the muscularis mucosae. This smooth muscle layer exhibited Ca2+ waves and flashes, but localized Ca2+ events (Ca2+ sparks, purinergic receptor-mediated transients) were not detected. Ca2+ flashes, often in bursts, occurred with a frequency (∼5.7/min) similar to that of SPCs (∼4/min), suggesting that SPCs are triggered by bursts of Ca2+ flashes. The force generated by a single mucosal SPC represented the maximal force of the strip, whereas a single detrusor SPC was ∼3% of maximal force of the detrusor strip. Electrical field stimulation (0.5–50 Hz) evoked force transients in isolated detrusor and mucosal strips. Inhibition of cholinergic receptors significantly decreased force in detrusor and mucosal strips (at higher frequencies). Concurrent inhibition of purinergic and cholinergic receptors nearly abolished evoked responses in detrusor and mucosae. Mucosal SPCs were unaffected by blocking small-conductance Ca2+-activated K+ (SK) channels with apamin and were unchanged by blocking large-conductance Ca2+-activated K+ (BK) channels with iberiotoxin (IbTX), indicating that SK and BK channels play a much smaller role in regulating muscularis mucosae SPCs than they do in regulating detrusor SPCs. Consistent with this, BK channel current density in myocytes from muscularis mucosae was ∼20% of that in detrusor myocytes. These findings indicate that the muscularis mucosae in guinea pig represents a second smooth muscle compartment that is physiologically and pharmacologically distinct from the detrusor and may contribute to the overall contractile properties of the urinary bladder.
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8

Al-Shukri, S. Kh, T. G. Giorgobiani, R. E. Amdiy e A. S. Al-Shukri. "Urinary dysfunction in patients with unsatisfactory results of surgical treatment of benign prostatic hyperplasia". Grekov's Bulletin of Surgery 176, n. 6 (28 dicembre 2017): 66–70. http://dx.doi.org/10.24884/0042-4625-2017-176-6-66-70.

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Abstract (sommario):
OBJECTIVE. The study aimed to develop diagnostics and treatment of urinary dysfunction in patients with unsatisfactory results of surgery of benign prostatic hyperplasia (BPH). MATERIAL AND METHODS. The urodynamic studies were made for 93 (72,7 %) patients after transurethral resection of the prostate and 35 (27,3 %) patients after open adenomectomy. All the patients had urinary dysfunctions after surgery of BPH. RESULTS. Detrusor hyperactivity was revealed in 51 (39,9 %) patients. Detrusor hypoactivity was noted in 21 (16,4 %) patients. Combination of detrusor hyperactivity during storage phase and detrusor hypoactivity during emptying phase had 25 (19,5 %) patients. Infravesical obstruction was detected in 22 (17,2 %). Urgent incontinence was diagnosed in 10 cases. There were 9 patients with signs of stress and condition combined with predomination of stress component. Treatment depended on the causes of urination dysfunction. CONCLUSIONS. Results of urodynamic studies allowed doctors to implement pathogenically verified therapy of urinary dysfunction after surgery of benign prostatic hyperplasia and improve its efficacy.
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9

Noronha, R., H. Akbarali, A. Malykhina, R. D. Foreman e Beverley Greenwood-Van Meerveld. "Changes in urinary bladder smooth muscle function in response to colonic inflammation". American Journal of Physiology-Renal Physiology 293, n. 5 (novembre 2007): F1461—F1467. http://dx.doi.org/10.1152/ajprenal.00311.2007.

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Abstract (sommario):
Visceral organ “cross talk” is suspected to contribute to multiorgan symptomatology found in conditions such as irritable bowel syndrome and interstitial cystitis. The goal of the present study was to investigate the short- and long-term effects of acute colitis on bladder detrusor muscle contractility. We hypothesized that inflammation of the colon leads to changes in bladder function via direct changes in detrusor smooth muscle contractility. In this study, colonic inflammation was induced in male rats via an enema of trinitrobenzenesulfonic acid (TNBS) (50 mg/kg, 0.5 ml, 25% ethanol). Colitis was confirmed using gross morphology, histology, and measurements of myeloperoxidase activity. Saline enema-treated rats served as controls. Three, 15, and 30 days postenema treatment, bladder detrusor muscle contractility was investigated in response to electrical field stimulation (EFS), cholinergic agonism with carbachol (CCh), and KCl. During active colonic inflammation ( day 3 post-TNBS enema), the bladder detrusor muscle appeared normal and showed no significant inflammation. However, abnormalities in bladder detrusor muscle contractility occurred in response to EFS and CCh but not KCl. During and after recovery from colonic inflammation ( days 15 and 30 post-TNBS enema), changes in bladder detrusor muscle contractility in response to EFS and CCh returned to control levels. We found that a transient colonic inflammatory insult significantly attenuates the amplitude of bladder detrusor muscle contractions in vitro, at least in part, through changes in cholinergic innervation, which are reversible after recovery from the colitis.
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10

Rusina, Yelena Ivanovna. "The role of complex preoperative urodynamic testing of continent women when planning surgery for pelvic organ prolapse". Journal of obstetrics and women's diseases 63, n. 1 (15 dicembre 2014): 17–25. http://dx.doi.org/10.17816/jowd63117-25.

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Abstract (sommario):
Women with significant genitourinary prolapse may be continent in spite of a weak urethral sphincter because of kinking of the poorly supported urethra. After the surgery for prolapse 19-30 % of the patients identify “occult” urinary incontinence due to a weak urethral sphincter. The aim of this study is to evaluate the role of complex urodynamic testing to identify “occult” urinary incontinence, neuromuscular dysfunction of the bladder and urethra for adequate combined therapy. Methods: 257 female patients with no urinary incontinence at the age of 30-86 years old were examined, before the surgery the pelvic organ prolapse of II-IV stages was reduced by Simps vaginal speculum: 102 women were clinically tested, and 155 women were complexly (clinically and urodynamically) evaluated. In addition to clinical examination urodynamic testing was made. Complex examination was repeated to all of them after 1-3 and 12-36 months after the operation. Results: Decrease of values of abdominal pressure transmission (APT) of less than 100 % was found significantly more often (38 ± 3.9 %) compared to a positive cough test while clinical exami-nation(19.4 ± 3.2 %) P < 0.001. Preoperatively detrusor overactivity was diagnosed in 12.5 ± 3.5 % and 11.8 ± 4.2 % cases, urethral instability - in 3.1 ± 1.7 % and 5.1 ± 2.8 % cases, detrusor sphincter dyssynergy - in 3.1 ± 1.7 % and 1.7 ± 1.6 % cases, detrusor hypotonia in 9.4 ± 3.0 % and 13.5 ± 4.4 % cases of patients with APT of more than 100 % and less than 100 % respectively. Patients with detrusor overactivity, urethral instability, detrusor hypotonya got medical preoperation treatment during 3 months and longer. 6 patients with detrusor-sphincter dyssynergy, detrusor hypotension were contraindicated for sling operation. Patients who had clinically and urodynamically confirmed urinary incontinence underwent simultaneous sling operations (13 women in a clinical group and 51 - in a complex group). In 12-36 months after the surgery no patient with APT of more than 100 % showed urinary incontinence. Clinically examined patients revealed totally 7 out of 102 (7.14 ± 2.5 %) complications after 12-36 months after surgery (mixed urinary incontinence in 4 cases and difunctional urination due to hypotonia detuzor in 3 cases). There are no these complications in the group of complexly examined women. Conclusions: Urodynamic testing can identify those women at risk of developing postoperative urinary incontinence and difunctional urination so that prophylactic measures can be undertaken. In cases when neuromuscular dysfunction is corrected and values of APT are less than 100 % simultaneous sling operation is reasonable.
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11

Radziszewski, P., R. Crayton, J. Zaborski, A. Członkowska, A. Borkowski, A. Bossowska e M. Majewski. "Multiple sclerosis produces significant changes in urinary bladder innervation which are partially reflected in the lower urinary tract functional status-sensory nerve fibers role in detrusor overactivity". Multiple Sclerosis Journal 15, n. 7 (19 giugno 2009): 860–68. http://dx.doi.org/10.1177/1352458509106210.

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Abstract (sommario):
Background Detrusor overactivity is often observed in patients with multiple sclerosis (MS), and neurotoxins are emerging as second-line therapies albeit with different degrees of success per patient basis. Objective To investigate lower urinary tract (LUT) functional status and bladder innervation (calcitonin gene related peptide [CGRP] and substance P [SP] positive nerve fibers) in patients with MS. Method Eighteen MS patients with LUT symptoms underwent urodynamic investigations, and six non-MS patients undergoing cystoscopy due to microscopic hematuria served as controls. Cold cut bladder biopsies were taken from the bladder trigone region. Neurotransmitter expression was determined by individual immunohistochemical staining. Results Two distinct groups could be distinguished: group 1 with pronounced neurogenic detrusor overactivity and mild outflow obstruction; group 2 with some degree of neurogenic detrusor overactivity, detrusor hypocontractility during voiding, and high degree of an outflow obstruction. The presence of SP and CGRP immunoreactive + fiber density was observed in greater numbers in group 1. Conclusion Density of CGRP and SP positive nerve fibers within the urinary bladder of patients with MS may be suggestive of functional status of the lower urinary tract, namely denser innervation is observed in patients with mild outflow obstruction and strong detrusor overactivity. This observation could be useful when planning second-line treatment (neurotoxins) in these patients. Patients with denser innervation probably will respond better to such a therapy.
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12

Ingargiola, G. B., M. Lamartina e A. Di Girolamo. "Urodynamics in urinary incontinence". Urologia Journal 65, n. 1 (febbraio 1998): 28–32. http://dx.doi.org/10.1177/039156039806500104.

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Abstract (sommario):
This study outlines the main urethral-bladder disorders responsible, on a neurological basis, for incontinence. It also defines the forms of detrusorial and urethral origin, due to hyper- or hypoactivity of the detrusor and urethra respectively. Brief reference is made to clinical aspects.
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13

Gad, Parag N., Nelly Kokikian, Kari L. Christe, V. Reggie Edgerton e Leif A. Havton. "Noninvasive neurophysiological mapping of the lower urinary tract in adult and aging rhesus macaques". Journal of Neurophysiology 119, n. 4 (1 aprile 2018): 1521–27. http://dx.doi.org/10.1152/jn.00840.2017.

Testo completo
Abstract (sommario):
The lower urinary tract (LUT) may be activated by spinal cord stimulation, but the physiological mapping characteristics of LUT activation with noninvasive transcutaneous spinal cord stimulation (TSCS) are not known. The effects of aging on the contractile properties of the detrusor are also not well understood. Therefore, TSCS was applied over the T10/T11 to L6/L7 spinous processes in adult ( n = 6) and aged ( n = 9) female rhesus macaques. A combination of urodynamic studies and electromyography recordings of the external urethral sphincter (EUS), external anal sphincter (EAS), and pelvic floor muscles was performed. Distinct functional maps were demonstrated for TSCS-evoked detrusor and urethral pressures and for the activation of the EUS, EAS, and pelvic floor muscles. The magnitude of responses for each peripheral target organ was dependent on TSCS location and strength. The strongest detrusor contraction was observed with TSCS at the L1/L2 site in adults and the L3/L4 site in aged subjects. TSCS-evoked bladder pressure at the L1/L2 site was significantly higher for the adults compared with the aged subjects ( P < 0.05). Cumulative normalized TSCS-evoked pressures, calculated for five consecutive sites between the T11/T12 and L3/L4 levels, were significantly lower for aged compared with adult subjects ( P < 0.05). The aged animals also showed a caudal shift for the TSCS site that generated the strongest detrusor contraction. We conclude that natural aging in rhesus macaques is associated with decreased detrusor contractility, a finding of significant translational research relevance as detrusor underactivity is a common occurrence with aging in humans. NEW & NOTEWORTHY Transcutaneous spinal cord stimulation (TSCS) was used to map lower urinary tract function in adult and aged rhesus macaques. Aging was associated with decreased peak pressure responses to TSCS, reduced cumulative normalized evoked bladder pressure responses, and a caudal shift for the site generating the strongest TSCS-induced detrusor contraction. We demonstrate the utility of TSCS as a new diagnostic tool for detrusor contractility assessments and conclude that aging is associated with decreased detrusor contractility in primates.
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14

Ballaro, Andrew. "The Elusive Electromyogram in the Overactive Bladder: A Spark of Understanding". Annals of The Royal College of Surgeons of England 90, n. 5 (luglio 2008): 362–67. http://dx.doi.org/10.1308/003588408x301217.

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Abstract (sommario):
It has been said that a technique capable of recording a urinary bladder electromyogram could be useful in the clinical evaluation of the detrusor neuropathies and myopathies implicated in the generation of lower urinary tract symptoms. However, in contrast to electromyography of skeletal and cardiac muscle, detrusor smooth muscle electromyography has remained in its infancy despite 50 years of scientific effort. The principal problems appear to be isolation of the real signal from artefacts, and the doubtful existence of electromyographic activity during cholinergic muscle contraction. The discovery of purinergic neuromuscular transmission in the overactive human bladder has renewed interest in detrusor electromyography as, in contrast to cholinergic mechanisms, purinergic mechanisms can generate extracellular electrical activity. In this paper, the development and validation of a novel technique for recording electrical activity from neurologically intact guinea-pig and human detrusor in vitro is described. A purinergic electromyographic signal is characterised and it is shown that detrusor taken from overactive human bladders has a greater propensity to generate electromyographic activity than normal by virtue of an aberrant purinergic mechanism.
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Smolnova, Tatyana Yu, e D. M. Lukyanova. "The role of genetic polymorphisms and growth factors in pathogenesis of urgent and mixed urinary incontinence in women". Medical Journal of the Russian Federation 22, n. 6 (15 dicembre 2016): 325–28. http://dx.doi.org/10.18821/0869-2106-2016-22-5-325-328.

Testo completo
Abstract (sommario):
The purpose of study. To analyze genetic polymorphisms of receptors of bladder, structural components of intercellular matrix of urinary excretion organs, molecular biochemical mechanisms of regulation of function of bladder and urethra resulting in urinary incontinency. Materials and methods. The analysis of publication data concerning genetic polymorphisms and molecular biochemical mechanisms of development of urinary incontinence in women. The results. The publication data is presented concerning impact of genetic polymorphisms of receptors of detrusor on development of urgent and mixed urinary incontinency in women. The corresponding molecular genetic and biochemical processes underlying detrusor sphincter dyssynergia in women are considered. Conclusion. The urinary incontinence is a multifactorial pathology developing due to alterations at systemic, organic, tissular and cellular levels. Such growth factors as bFGF, TGFβ, CTGF contribute into pathogenesis of urgent and partially mixed urinary incontinency resulting in intensification of unstripped muscle cohesions of detrusor, obstructive miohypertrophy and fibrosis of bladder wall. The altered adrenalin reactivity of urinary excretion ways plays particular role in pathogenesis of urgent component of urinary incontinence. And vice versa, damage of structure of connective tissue in patients with polymorphism COL1A1 or disorder of molecular biochemical mechanism of action of cytokines TGFβ and CTGF provoke insufficiency of sphincter apparatus of urinary excretion ways. The totality of enumerated mechanisms results in development of stress urinary incontinency. The elaboration of individual approach to selection of treatment method requires consideration of mentioned mechanisms of development of urinary incontinence including form and severity of disease.
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Islianti, Putri Iradita, Harrina Erlianti Rahardjo, Nur Rasyid e Arry Rodjani. "PREVALENCE OF LOWER URINARY TRACT SYMPTOMS POST KIDNEY TRANSPLANTATION AND ITS URODYNAMIC PROFILE". Indonesian Journal of Urology 28, n. 2 (15 luglio 2021): 158–63. http://dx.doi.org/10.32421/juri.v28i2.683.

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Abstract (sommario):
Objective: This study aimed to describe the urodynamic characteristics of post-transplant kidney patients with LUTS who were indicated for urodynamics. Material & Methods: This research is a cross-sectional study conducted at Cipto Mangunkusumo General Hospital between 2011-2017. Data were collected from patients who had undergone urodynamic examination after kidney transplantation due to LUTS/urinary retention. Data were collected from the patient’s medical record. Results: A total of 536 patients underwent kidney transplants at Cipto Mangunkusumo General Hospital from 2011-2017. Eleven patients (2%) developed LUTS and then underwent urodynamic examination with an average age of 41.4 (30.1 ± 52.6) years. Six patients (55%) had type 2 diabetes mellitus (DM) and 5 patients (45%) had hypertension (HT). A total of 6 out of 11 patients (54%) experienced urinary retention of which 4 subjects (67%) had decreased bladder compliance, 4 (67%) patients experienced detrusor overactivity (DO), 3 patients (50%) had bladder outlet obstruction (BOO), while 2 patients (33%) experienced detrusor underactivity (DU) respectively. Of 5 patients without urinary retention, decreased bladder compliance was found in 1 patient (20%), DO in 2 patients (40%), BOO in 1 patient (20%), and no subject experienced DU. In both groups, no subject was discovered to experience any urinary incontinence. Conclusion: Small number of post renal transplantation patients developed LUTS and half of which accompanied by urinary retention. Among these patients, urodynamic examination revealed detrusor overactivity as the most common underlying problem followed by decreased bladder compliance, BOO, and detrusor underactivity
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CALVERT, Robert C., Faiz H. MUMTAZ, Mick R. DASHWOOD, Masood A. KHAN, Robert J. MORGAN, Dimitri P. MIKHAILIDIS e Cecil S. THOMPSON. "Reduction of endothelin-1 binding and inhibition of endothelin-1-mediated detrusor contraction by naftidrofuryl". Clinical Science 103, s2002 (1 settembre 2002): 459S—463S. http://dx.doi.org/10.1042/cs103s459s.

Testo completo
Abstract (sommario):
Endothelin-1 (ET-1) causes urinary bladder smooth muscle contraction and the endothelin receptors A and B (ETA and ETB) are both known to be present in the rabbit urinary bladder. Alterations in ET-1 signalling have been implicated in the pathophysiology of urinary tract disorders secondary to bladder outlet obstruction and also in diabetic cystopathy. Naftidrofuryl (Naf) (marketed under the trade name Praxilene) improves walking distance in patients with peripheral vascular disease, an effect which may be partially attributed to ET-1 antagonism. The purpose of this study is to assess whether Naf will reduce ET-1 binding in the rabbit detrusor muscle and to assess whether there is inhibition of ET-1-mediated detrusor contraction. Detrusor smooth muscle strips were mounted in organ baths and cumulative response curves were measured for ET-1-mediated contractions in the presence and absence of 10-6M Naf (therapeutic concentration). In addition, ET-1 was added to the detrusor strips in the presence of the ETA antagonist, BQ123, and the ETB antagonist, BQ788, to identify the receptor subtype functionally involved. Overall inhibition of [125I]ET-1 binding by Naf was assessed using autoradiography. Identification of receptor-subtype binding reduction was assessed using the radioligands [125I]PD151242 and [125I]BQ3020. Naf inhibited ET-1-mediated detrusor contractions significantly (P<0.04), e.g. at 10-10M ET-1, contraction was completely abolished by Naf. Autoradiography indicated that Naf competitively inhibited [125I]ET-1 binding in a dose-dependent manner (IC50 = 3×10-7M). All radioligand binding was reduced indicating binding of Naf to both ETA and ETB receptors. Naf reduces binding of ET-1 to rabbit detrusor ETA and ETB receptors and inhibits ET-1-induced detrusor contractions mediated by ETA receptors. Naf may have therapeutic potential in the treatment of bladder disorders secondary to bladder outlet obstruction and diabetes mellitus.
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18

Klinger, Mary Beth, Abbey Dattilio e Margaret A. Vizzard. "Expression of cyclooxygenase-2 in urinary bladder in rats with cyclophosphamide-induced cystitis". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, n. 2 (agosto 2007): R677—R685. http://dx.doi.org/10.1152/ajpregu.00305.2007.

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Abstract (sommario):
These studies examined the expression of cyclooxygenase-2 (COX-2) expression in the urothelium and suburothelial space and detrusor from rats treated with cyclophosphamide (CYP) to induce acute (4 h), intermediate (48 h), or chronic (10-day) cystitis. Western blot analysis and immunohistochemistry were used to demonstrate COX-2 expression. In whole mount preparations of urinary bladder, nerve fibers in the suburothelial plexus, and inflammatory cell infiltrates were characterized for COX-2 expression after CYP-induced cystitis. COX-2 expression significantly ( P ≤ 0.01) increased in the urothelium + suburothelium and detrusor smooth muscle with acute, intermediate, and chronic (10-day) CYP-induced cystitis, but expression in urothelium + suburothelium was significantly greater. CYP-induced upregulation of COX-2 showed by immunostaining in the urothelium + suburothelium was similar to that observed with Western blot analysis and also demonstrated COX-2 inflammatory cell infiltrates (CD86+) and nerve fibers (PGP+) in the suburothelial plexus. Although COX-2 expression was significantly ( P ≤ 0.01) increased in detrusor smooth muscle, immunohistochemistry failed to demonstrate an obvious change in COX-2-immunoreactivity (IR) in detrusor muscle, but COX-2 inflammatory infiltrates were present throughout the detrusor. COX-2-IR nerve fibers exhibited increased density in the suburothelial plexus with acute or chronic CYP-induced cystitis. COX-2-IR macrophages (CD86+) were present throughout the urinary bladder with acute and chronic CYP-induced cystitis. These studies demonstrate cellular targets in the urinary bladder where COX-2 inhibitors may act.
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19

Minaldi, G., B. Ventimiglia, M. Finocchiaro, I. Fanzone, A. Tsirgiotis, F. Spitaleri, G. Di Marco e S. Ranno. "Sexual Activity and Urinary Incontinence in Women". Urologia Journal 76, n. 3 (luglio 2009): 203–6. http://dx.doi.org/10.1177/039156030907600306.

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Abstract (sommario):
Urinary incontinence during sexual intercourse refers to overactive bladder (OAB) syndrome and it is divided in incontinence during penetration and during orgasm. 480 women with low urinary tract symptoms (LUTS) were divided in a) affected by probable genuine stress incontinence, b) probable Urge-stress incontinence, c) probable Urge Incontinence, to specify incidence. Materials and Methods In Group C (186 women) 36 women, age range 24 to 56 years, with urinary incontinence only during sexual intercourse, were selected: 16 during orgasm (group I), 20 during penetration (group II). These patients filled in specific validated questionnaires (ICI-9), urinary recordings and, after urine exam, they underwent US study of urinary tract with post-micturition evaluation. The patients with other urological diseases or pelvic prolapse in stage II of POP-Q or higher were excluded. Patients were referred to physiatric evaluation and urodynamic exam with cystomanometry and perineal EMG, with provocative tests and after pressure-flow study. Results Cystocele was found in 4 out of 16 women in Group I, and in 6 out of 20 in Group II. No patients showed basic detrusor hyperactivity during cystomanometry. In Group I: 50% had detrusor hyperactivity and 18.75% had prolonged perineal relaxation. In Group II 30% had detrusor hyperactivity and 35% had prolonged perineal deficit. Results suggest parasympathetic deficiency in Group I and sympathetic deficiency in Group II.
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20

LaBerge, Jennifer, Susan E. Malley, Katarina Zvarova e Margaret A. Vizzard. "Expression of corticotropin-releasing factor and CRF receptors in micturition pathways after cyclophosphamide-induced cystitis". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, n. 3 (settembre 2006): R692—R703. http://dx.doi.org/10.1152/ajpregu.00086.2006.

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Abstract (sommario):
Corticotropin-releasing factor (CRF) is a prominent neuropeptide involved in micturition reflexes, and different roles in these reflexes have been suggested. These studies examined the expression of CRF in the urinary bladder and lumbosacral sacral parasympathetic nucleus (SPN) in response to cyclophosphamide (CYP)-induced cystitis (4 h, 48 h, or chronic) in rats. The expression of CRF receptors, CRF1 and CRF2, was examined in urinary bladder from control and CYP-treated rats. Urinary bladder and lumbosacral spinal cord were harvested from rats killed by isoflurane (4%) and thoracotomy. CRF protein expression in whole urinary bladders significantly ( P ≤ 0.01) increased with 48 h or chronic CYP treatment. CRF immunoreactivity (IR) was increased significantly ( P ≤ 0.01) in the urothelium and SPN after CYP treatment. CRF IR nerve fibers increased in density in the suburothelial plexus and detrusor smooth muscle whole mounts with CYP-induced cystitis. CRF2 receptor transcript was expressed in the urothelium or detrusor smooth muscle, and CRF2 receptor expression increased in whole bladder with CYP-treatment, whereas no CRF1 receptor transcript was expressed in either urothelium or detrusor. Immunohistochemical studies demonstrated CRF2 IR in urinary bladder nerve fibers and urothelial cells from control animals, whereas no CRF1 IR was observed. These studies demonstrated changes in the expression of CRF in urinary bladder and SPN region with CYP-induced cystitis and CRF receptor (CRF2) expression in nerve fibers and urothelium in control rats. CRF may contribute to urinary bladder overactivity and altered sensory processing with CYP-induced cystitis.
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21

Chung, Doreen E., Benjamin Dillon, Jordan Kurta, Alexandra Maschino e Jaspreet S. Sandhu. "Detrusor underactivity is prevalent after radical prostatectomy: A urodynamic study including risk factors". Canadian Urological Association Journal 7, n. 1-2 (23 gennaio 2013): 33. http://dx.doi.org/10.5489/cuaj.192.

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Abstract (sommario):
Introduction: The objective was to determine the prevalence of, and factors that predict, detrusor underactivity (DU) in patients presenting with incontinence or lower urinary tract symptoms (LUTS) following radical prostatectomy (RP). We also determined the prevalence of bladder outlet obstruction (BOO) and detrusor overactivity (DO) in this population.Methods: Patients who underwent urodynamics post-RP were identified. Detrusor underactivity was defined as a maximum flow rate (Qmax) of ≤15 mL/s and detrusor pressure (Pdet) Qmax <20 cmH20 or maximum Pdet <20 cmH20 during attempted voiding. Abdominal voiding (AV) was defined as sustained increase in abdominal pressure during voiding. Bladder outlet obstruction and DO were identified using the Abrams-Griffiths nomogram and the International Continence Society criteria. Univariate logistic regression was used to determine factors predicting DU. The following factors were analyzed: age, year of RP, procedure type (minimally-invasive surgery [MIS] or open), postoperative radiation, nerve-sparing, clinical stage, biopsy Gleason grade and interval between RP and evaluation.Results: Between 2005 and 2008, 264 patients underwent urodynamics post-RP. Detrusor underactivity was observed in 108 patients (41%; 95% CI 35%, 47%), of whom 48% demonstrated AV. Overall, BOO and DO were present in 17% (95% CI 12%, 22%) and 27% (95% CI 22%, 33%), respectively. On univariate analysis, only MIS RP was predictive of DU (univariate odds ratio 2.05 for MIS vs. open; p = 0.009).Conclusions: Detrusor underactivity and AV are common in patients presenting for evaluation of incontinence or LUTS following RP. The etiology of DU in this setting is likely related to the surgical approach. Because DU may affect the success of male incontinence treatment with the male sling or artificial urinary sphincter, it is useful to document its presence prior to treatment. More studies are needed to elucidate the influence of DU on treatment success for male urinary incontinence following RP.
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22

Dorsher, Peter T., e Peter M. McIntosh. "Neurogenic Bladder". Advances in Urology 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/816274.

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Abstract (sommario):
Congenital anomalies such as meningomyelocele and diseases/damage of the central, peripheral, or autonomic nervous systems may produce neurogenic bladder dysfunction, which untreated can result in progressive renal damage, adverse physical effects including decubiti and urinary tract infections, and psychological and social sequelae related to urinary incontinence. A comprehensive bladder-retraining program that incorporates appropriate education, training, medication, and surgical interventions can mitigate the adverse consequences of neurogenic bladder dysfunction and improve both quantity and quality of life. The goals of bladder retraining for neurogenic bladder dysfunction are prevention of urinary incontinence, urinary tract infections, detrusor overdistension, and progressive upper urinary tract damage due to chronic, excessive detrusor pressures. Understanding the physiology and pathophysiology of micturition is essential to select appropriate pharmacologic and surgical interventions to achieve these goals. Future perspectives on potential pharmacological, surgical, and regenerative medicine options for treating neurogenic bladder dysfunction are also presented.
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23

Gonzalez, Eric J., e Warren M. Grill. "The effects of neuromodulation in a novel obese-prone rat model of detrusor underactivity". American Journal of Physiology-Renal Physiology 313, n. 3 (1 settembre 2017): F815—F825. http://dx.doi.org/10.1152/ajprenal.00242.2017.

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Abstract (sommario):
Obesity is a global epidemic associated with an increased risk for lower urinary tract dysfunction. Inefficient voiding and urinary retention may arise in late-stage obesity when the expulsive force of the detrusor smooth muscle cannot overcome outlet resistance. Detrusor underactivity (DUA) and impaired contractility may contribute to the pathogenesis of nonobstructive urinary retention. We used cystometry and electrical stimulation of peripheral nerves (pudendal and pelvic nerves) to characterize and improve bladder function in urethane-anesthetized obese-prone (OP) and obese-resistant (OR) rats following diet-induced obesity (DIO). OP rats exhibited urinary retention and impaired detrusor contractility following DIO, reflected as increased volume threshold, decreased peak micturition pressure, and decreased voiding efficiency (VE) compared with OR rats. Electrical stimulation of the sensory branch of the pudendal nerve did not increase VE, whereas patterned bursting stimulation of the motor branch of the pudendal nerve increased VE twofold in OP rats. OP rats required increased amplitude of electrical stimulation of the pelvic nerve to elicit bladder contractions, and maximum evoked bladder contraction amplitudes were decreased relative to OR rats. Collectively, these studies characterize a novel animal model of DUA that can be used to determine pathophysiology and suggest that neuromodulation is a potential management option for DUA.
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24

Reinfeldt Engberg, Gisela, Clara Ibel Chamorro, Agneta Nordenskjöld e Magdalena Fossum. "Expansion of Submucosal Bladder Wall TissueIn VitroandIn Vivo". BioMed Research International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/5415012.

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Abstract (sommario):
In order to develop autologous tissue engineering of the whole wall in the urinary excretory system, we studied the regenerative capacity of the muscular bladder wall. Smooth muscle cell expansion on minced detrusor musclein vitroandin vivowith or without urothelial tissue was studied. Porcine minced detrusor muscle and urothelium were culturedin vitrounder standard culture conditions for evaluation of the explant technique and in collagen for tissue sectioning and histology. Autografts of minced detrusor muscle with or without minced urothelium were expanded on 3D cylinder moulds by grafting into the subcutaneous fat of the pig abdominal wall. Moulds without autografts were used as controls. Tissue harvesting, mincing, and transplantation were performed as a one-step procedure. Cells from minced detrusor muscle specimens migrated and expandedin vitroon culture plastic and in collagen.In vivostudies with minced detrusor autografts demonstrated expansion and regeneration in all specimens. Minced urothelium autografts showed multilayered transitional urothelium when transplanted alone but not in cotransplantation with detrusor muscle; thus, minced bladder mucosa was not favored by cografting with minced detrusor. No regeneration of smooth muscle or epithelium was seen in controls.
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25

Bing, Wu, Shaohua Chang, Joseph A. Hypolite, Michael E. DiSanto, Stephen A. Zderic, Lester Rolf, Alan J. Wein e Samuel Chacko. "Obstruction-induced changes in urinary bladder smooth muscle contractility: a role for Rho kinase". American Journal of Physiology-Renal Physiology 285, n. 5 (novembre 2003): F990—F997. http://dx.doi.org/10.1152/ajprenal.00378.2002.

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Abstract (sommario):
Detrusor smooth muscle (DSM) undergoes hypertrophy after partial bladder outlet obstruction (PBOO) in male rabbits, as it does in men with PBOO induced by benign prostatic hyperplasia. Despite detrusor hypertrophy, some bladders are severely dysfunctional (decompensated). In this study, the rabbit model for PBOO was used to determine the biochemical regulation of the contractile apparatus and force maintenance by the detrusor from decompensated bladders (DB). Bladders from sham-operated rabbits served as a control. On stimulation with 125 mM KCl, the DSM from sham-operated (SB) rabbits showed phasic contractions, whereas the detrusor from DB was tonic, exhibiting slow development of force, a longer duration of force maintenance, and slow relaxation. The Rho kinase (ROK) inhibitor Y-27632 enhanced the relaxation of precontracted DSM strips from DB. The enhancement of relaxation of the KCl-induced contraction of DB by Y-27632 was associated with dephosphorylation of myosin light chain (MLC20). The DSM extract from DB showed low phosphatase activity compared with that from SB. The DB also showed more Ca2+-independent MLC20 phosphorylation, which was partially inhibited by Y-27632. RT-PCR and Western blotting revealed similar expression levels of MLC kinase and ROK-α in SB and DB, but ROK-β was overexpressed in DB. These results suggest that the ROK-mediated pathway is partly responsible for the high degree of force maintenance and slow relaxation in the detrusor from DB.
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26

Kawata, Ryoya, Yuji Hotta, Kotomi Maeda, Tomoya Kataoka e Kazunori Kimura. "Effects of High Salt Intake on Detrusor Muscle Contraction in Dahl Salt-Sensitive Rats". Nutrients 13, n. 2 (7 febbraio 2021): 539. http://dx.doi.org/10.3390/nu13020539.

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Abstract (sommario):
High salt intake has been reported as a risk factor for urinary storage symptoms. However, the association between high salt intake and detrusor muscle contraction is not clear. Therefore, we investigated the effects of high salt intake on the components of detrusor muscle contraction in rats. Six-week-old male Dahl salt-resistant (DR; n = 5) and Dahl salt-sensitive (DS; n = 5) rats were fed a high salt (8% NaCl) diet for one week. The contractile responses of the detrusor muscle to the cumulative administration of carbachol and electrical field stimulation (EFS) with and without suramin and atropine were evaluated via isometric tension study. The concentration–response curves of carbachol were shifted more to the left in the DS group than those in the DR group. Contractile responses to EFS were more enhanced in the DS group than those in the DR group (p < 0.05). Cholinergic component-induced responses were more enhanced in the DS group than those in the DR group (p < 0.05). High salt intake might cause urinary storage symptoms via abnormalities in detrusor muscle contraction and the enhancement of cholinergic signals. Excessive salt intake should be avoided to preserve bladder function.
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27

Gomes, Cristiano M., Sami Arap e Flávio E. Trigo-Rocha. "Voiding dysfunction and urodynamic abnormalities in elderly patients". Revista do Hospital das Clínicas 59, n. 4 (2004): 206–15. http://dx.doi.org/10.1590/s0041-87812004000400010.

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Abstract (sommario):
Lower urinary tract dysfunction is a major cause of morbidity and decreased quality of life in elderly men and women. With the progressive aging of the population, it is important to understand common micturitional disorders that may occur in this population. Most urinary problems in the elderly are multifactorial in origin, demanding a comprehensive assessment of the lower urinary tract organs, functional impairments, and concurrent medical diseases. Urodynamics is a highly valuable tool in the investigation of elderly patients with lower urinary tract symptoms. Urodynamic tests are not always necessary, being indicated after excluding potentially reversible conditions outside the urinary tract that may be causing or contributing to the symptoms. Although urodynamic tests may reveal common diagnoses such as bladder outlet obstruction and stress urinary incontinence in the elderly population, findings such as detrusor overactivity and impaired detrusor contractility are common and have important prognostic and therapeutic implications. The purpose of this article is to describe common urologic problems in the elderly and review the indications for and clinical aspects of urodynamic studies in these conditions.
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28

KENI, LAXMIKANT G., SAGAR KALBURGI, B. M. ZEESHAN HAMEED, MOHAMMAD ZUBER, MASAAKI TAMAGAWA e B. SATISH SHENOY. "FINITE ELEMENT ANALYSIS OF URINARY BLADDER WALL THICKNESS AT DIFFERENT PRESSURE CONDITION". Journal of Mechanics in Medicine and Biology 19, n. 05 (agosto 2019): 1950029. http://dx.doi.org/10.1142/s0219519419500295.

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Abstract (sommario):
In this work, a 3D urinary bladder was subjected to various pressure loading conditions mimicking the bladder filling volume. The bladder layer consisting of adventitia, detrusor and mucosa layer having different mechanical properties produced different deformation and stresses when subjected to the varying loads. The volume of the bladder changed to 231.34[Formula: see text]ml which was 128.91% higher than the assumed initial volume of 50[Formula: see text]ml on application of 18[Formula: see text]kPa of pressure. The detrusor layer which is thickest of the bladder wall reduced to 1.312[Formula: see text]mm from 4.4[Formula: see text]mm, recording a 108% change in its thickness at 18[Formula: see text]kPa pressure. The maximum von-Mises stress obtained were significantly higher in case of the Mucosa layer when compared to the detrusor and adventia layer. The unique layup of the bladder wall having different properties plays a major role in sustaining adverse pressure gradients and absorbing high stresses.
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29

Jiang, Yuan-Hong, Sheng-Fu Chen e Hann-Chorng Kuo. "Frontiers in the Clinical Applications of Botulinum Toxin A as Treatment for Neurogenic Lower Urinary Tract Dysfunction". International Neurourology Journal 24, n. 4 (31 dicembre 2020): 301–12. http://dx.doi.org/10.5213/inj.2040354.177.

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Abstract (sommario):
Patients with neurogenic lower urinary tract dysfunction (NLUTD) experience urinary incontinence with or without difficult urination, which might promote recurrent urinary tract infection (UTI) and exacerbate upper urinary tract function. Nonetheless, appropriate bladder management has been shown to reduce urological complications and improve quality of life. In addition to pharmacological therapy and surgical intervention, botulinum toxin A (BoNT-A) has been widely utilized in NLUTD. The therapeutic efficacy of detrusor BoNT-A injections for neurogenic detrusor overactivity due to spinal cord injury (SCI), multiple sclerosis, or other central nervous system lesions, such as cerebrovascular accident, Parkinson disease, early dementia, and pediatric NLUTD due to myelomeningocele, has been well established, with repeated BoNT-A injections every 6 to 9 months being necessary to maintain its therapeutic effects. Urethral BoNT-A injection can decrease urethral sphincter resistance and facilitate efficient voiding in patients with NLUTD who wish to preserve self-voiding. Detrusor BoNT-A injection can also decrease the occurrence of autonomic dysreflexia in patients with SCI, even after failed augmentation enterocystoplasty, with additional benefits including reduced UTI episodes and preserved renal function with repeated injections. However, this treatment does have some side effects. Complete informed consent for BoNT-A injection therapy with full disclosure of its potential complications should therefore be obtained before this procedure is undertaken.
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30

Ghirca, Veronica Maria, D. Porav-Hodade, C. Chibelean, S. Voidazan, M. Vartolomei, R. Boja e Orsolya Martha. "The Role of Urodynamic Investigations in Management of Stress Urinary Incontinence". Acta Medica Marisiensis 61, n. 4 (1 dicembre 2015): 298–302. http://dx.doi.org/10.1515/amma-2015-0115.

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Abstract (sommario):
AbstractObjective: The aim of this study is to establish the importance of urodynamic investigations in women diagnosed with stress urinary incontinence (SUI) who have indication of surgical treatment.Methods: We performed a retrospective study over a period of 3 years (January 2012-December 2014) in Clinic of Urology from Tirgu Mures. The inclusion criteria were: female patients diagnosed with SUI having indication of surgical treatment and the existence of urodynamic investigations (uroflowmetry and pressure-flow study). We evaluated 118 patients with SUI. From this patients, 24 cases (20.3%) accomplished the criteria from above.Results: We included in this study 24 patients aged 64.25+/−8.25 (standard deviation). Pressure-flow study revealed an impaired detrusor contraction in 13 cases. Statistical anaysis pouved a relation between existence of post void residual urine (PVR) and underactive detrusor (UD) (p=0.01). There is no correlation between maximum flow rate (Qmax) and UD, r=0.18 (CI= −0.2-0.5), p=0.3 and between normal value of Qmax and normal detrusor pressure (Pdet), r= 0,28(CI=−0.6-0.8), p=0.58. Also there is no relation between a low Qmax and UD, p=0,5. There is a statistical relation between increased abdominal pressure (Pabd) and UD, p=0.02.Conclusions: Uroflowmetry has the role to guide us concerning the micturition process Pressure-flow study is indicated in management of SUI, in selected cases, in patients with voiding symptomatology, the suspicion of a detrusor contractility dysfunction, abnormal uroflowmetry results, existence of PVR, in prediction of the surgical treatment outcome or if we think that the findings can change the choice of treatment.
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31

Silva, Fabio Henrique, Celso Saragosa Ramos Filho, Fabiano Beraldi Calmasini, Eduardo Costa Alexandre, Roger Barbosa Ferreira, Mariana Goncalves de Oliveira, Mário Angelo Claudino, Carla Fernanda Franco-Penteado, Edson Antunes e Fernando F. Costa. "Oxidative Stress Contributes to Overactive Bladder in the Transgenic Sickle Cell Mouse". Blood 126, n. 23 (3 dicembre 2015): 4582. http://dx.doi.org/10.1182/blood.v126.23.4582.4582.

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Abstract (sommario):
Abstract Introduction: Lower urinary tract symptoms (LUTS) such as nocturia, urinary frequency, and urgency have been clinically reported in children and adults with sickle cell disease (SCD; Portocarrero et al J Urol 2012; Anele et al Neurourol Urodyn 2015), but little is known about the pathophysiology of micturition dysfunction in SCD patients. Transgenic sickle cell mice have been employed to better understand SCD pathophysiology. Recently, we reported that Berkeley SCD mice display underactive bladder and reduced detrusor smooth muscle contractions (Claudino et al Plos One, 2015). The homozygous Townes transgenic sickle cell mouse is another model for SCD, but urinary bladder dysfunction has never been studied in this model. Considering that SCD is associated with elevated ROS production, we hypothesized that increased ROS levels lead to alterations in the urinary bladder function of Townes SCD mice. Thus, the aim of this study was to evaluate the micturition and detrusor smooth muscle contractions in Townes transgenic sickle cell mice. Methods: Townes transgenic sickle cell mice and C57BL/6 mice (control) aged 3 to 4 months old were used. Cystometry was performed to evaluate the urinary function in vivo. In separate protocols, the urinary bladder was removed and placed in Krebs solution. Two longitudinal detrusor smooth muscle strips with intact urothelium were obtained from each bladder. The strips were mounted in 4-ml organ baths containing Krebs-Henseleit solution at 37°C continuously bubbled with a mixture of 95% O2 and 5% CO2 (pH 7.4). Cumulative concentration-response curves to muscarinic receptor agonist carbachol (CCh; 0.01-100 μM), chloride potassium (KCl; 1-300mM) and frequency-response curves for electrical field stimulation (EFS; 1-32Hz) were obtained in strips of detrusor smooth muscle from both control and SCD mice.mRNA expression for gp91phox and SOD-1 in bladder were also evaluated. Results: Micturition in SCD mice was irregular, and characterized by significant (P < 0.05) increases in the frequency of voiding contractions and nonvoiding contractions (n=5). Voiding pressure, basal pressure, capacity and threshold pressure were not changed in SCD mice. Carbachol (0.01 - 100 µM) induced concentration-dependent detrusor smooth muscle contractions in both control and SCD mice, but maximal contractile responses were significantly lower (P < 0.05) in SCD compared to control mice (1.40 ± 0.4 and 2.9 ± 0.2 mN/mg, respectively; n=5). Likewise, EFS-induced neurogenic detrusor contractions in SCD mice were 29% lower (P < 0.05) compared to the control (n=10). Contractile responses induced by KCl (1 - 300 mM) did not differ between control and SCD group (n=5). The mRNA expression for the NADPH subunit gp91phox in bladder was about 2-fold higher (P<0.05) in SCD mice compared to the control group, whereas no changes in the mRNA expression for SOD-1 were observed among groups (n=6). Infiltration by inflammatory cells (mononuclear cells) was seen in the submucosa and muscular area of bladder from SCD mice (n=4). Conclusion: Our study shows that the overactive bladder seen in SCD mouse is associated with upregulation of NADPH oxidase subunit gp91phox. Interestingly, in the contrast, the Berkeley SCD mouse exhibits an atonic detrusor smooth muscle and underactive bladder (Claudino et al Plos One 2015). One may speculate therefore that the overactive bladder in Townes SCD may progress to underactive bladder at latter stages. To confirm this hypothesis, we will evaluate the urinary bladder function in older SCD mice. Financial Support: FAPESP Disclosures No relevant conflicts of interest to declare.
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32

Weng, Te I., Hsiao Yi Wu, Pei Ying Lin e Shing Hwa Liu. "Uropathogenic Escherichia coli-Induced Inflammation Alters Mouse Urinary Bladder Contraction via an Interleukin-6-Activated Inducible Nitric Oxide Synthase-Related Pathway". Infection and Immunity 77, n. 8 (26 maggio 2009): 3312–19. http://dx.doi.org/10.1128/iai.00013-09.

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Abstract (sommario):
ABSTRACT Escherichia coli is the most common cause of urinary tract infection. Elevated blood and urine interleukin-6 (IL-6) levels have been shown in inflammatory urinary tract diseases. The role of IL-6 in mediating the urodynamic dysfunction in response to E. coli-induced urinary tract infection has not yet been fully elucidated. In this study, we investigated the role of IL-6 in the nitric oxide (NO)-triggered alteration of contractile responses in the urinary bladder under an E. coli-induced inflammatory condition. The electrical field stimulation (EFS)-evoked contractions of the isolated detrusor strips, and immunoblotting for detecting protein expression in the bladders was measured short term (1 h) or long term (6 or 24 h) after intraperitoneal injection of E. coli endotoxin (lipopolysaccharide [LPS]) or intravesical instillation of human pyelonephritogenic E. coli-J96 (O4:K6) strain or LPS into mice. IL-6 and NO productions were increased in the urinary bladders of mice 1 to 24 h after LPS or E. coli-J96 treatment. Inducible NO synthase (iNOS) expression and protein kinase C (PKC) activation and EFS-evoked detrusor contractions were increased in the bladders at 6 h after LPS or E. coli-J96 treatment, which could be reversed by anti-IL-6 antibody and iNOS inhibitor aminoguanidine. At 1 h after LPS administration, bladder NO generation, endothelial NOS expression, and EFS-evoked detrusor contractions were effectively increased, whereas anti-IL-6 antibody could not reverse these LPS-induced responses. These results indicate that IL-6 may play an important role in the iNOS/NO-triggered PKC-activated contractile response in urinary bladder during E. coli or LPS-induced inflammation.
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33

Romine, Mary T., e Gordon F. Anderson. "Evidence for oxytocin receptors in the urinary bladder of the rabbit". Canadian Journal of Physiology and Pharmacology 63, n. 4 (1 aprile 1985): 287–91. http://dx.doi.org/10.1139/y85-052.

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Abstract (sommario):
Experiments were performed on isolated detrusor smooth muscle from New Zealand White rabbits. Oxytocin was shown to exhibit high intrinsic contractile activity on isolated strips of detrusor muscle, where the maximum contractile amplitude was 12% greater than control responses to 1 μM carbachol. Repeated applications of 1 μM oxytocin were associated with tachyphylaxis representing a 49% decrease in the amplitude which became reproducible after several applications without further decay of contractile strength. Dose–response experiments indicated that threshold contractions to oxytocin occur at 3 μM and were maximum at 10 μM with mean effective concentration of 125 μM. The contractile responses to 1 μM oxytocin were not antagonized by phentolamine, atropine, methysergide, saralasin, or naloxone, but were partially inhibited by 1 μM of indomethacin. Ligand binding studies on partially purified membrane preparations from detrusor smooth muscle were performed over a range of 78 pM to 10 nM with 125I-labelled oxytocin. Scatchard analysis of specific bound receptors indicated a KD of 2.5 nM and Bmax of 187 fmol/mg protein and a second compartment that was unsaturable at the concentrations of ligand employed. Nonspecific binding ranged from 36 to 77% of the total binding.
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34

Bertapelle, Paola, Giovanni Bodo e Roberto Carone. "Detrusor Acontractility in Urinary Retention: Detrusor Contractility Test as Exclusion Criteria for Sacral Neurostimulation". Journal of Urology 180, n. 1 (luglio 2008): 215–16. http://dx.doi.org/10.1016/j.juro.2008.03.054.

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35

Hui, C., X. Keji, J. Chonghe, T. Ping, O. Rubiao, Z. Jianweng, D. Xiangrong et al. "Combined detrusor-trigone BTX-A injections for urinary incontinence secondary to neurogenic detrusor overactivity". Spinal Cord 54, n. 1 (11 agosto 2015): 46–50. http://dx.doi.org/10.1038/sc.2015.143.

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36

de Sèze, Marianne, Alain Ruffion, Pierre Denys, Pierre-Alain Joseph e Brigitte Perrouin-Verbe. "The neurogenic bladder in multiple sclerosis: review of the literature and proposal of management guidelines". Multiple Sclerosis Journal 13, n. 7 (15 marzo 2007): 915–28. http://dx.doi.org/10.1177/1352458506075651.

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Abstract (sommario):
Vesicourethral dysfunction is very frequent in multiple sclerosis (MS) and has functional consequences for patients' quality of life and also an organic impact following complications of the neurogenic bladder on the upper urinary tract. While the functional impact and its management are well documented in the literature, the organic impact remains underestimated and there are no consensual practical guidelines for the screening and prevention of MS neurogenic bladder complications. The aim of this review of the literature, focused on identifying the risk factors of urinary tract complications in MS, is to put forward well informed considerations to help in the definition of practical guidelines for the follow-up of the neurogenic bladder in MS in order to improve its prevention and patient management. Four main risk factors have been identified for upper urinary tract damage: the duration of MS, the presence of an indwelling catheter, high-amplitude neurogenic detrusor contractions and permanent high detrusor pressure. Detrusor-sphincter dyssynergia, age over 50 and male sex may form three additional risk factors. Recommendations for long-term urological follow-up, taking into account these specific risks are constructed according to the procedures recommended by the French Health Authorities. Multiple Sclerosis 2007; 13: 915-928. http://msj.sagepub.com
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37

Wu, Wei-Yi, Shih-Pin Lee, Bing-Juin Chiang, Wei-Yu Lin e Chiang-Ting Chien. "Urothelial Calcium-Sensing Receptor Modulates Micturition Function via Mediating Detrusor Activity and Ameliorates Bladder Hyperactivity in Rats". Pharmaceuticals 14, n. 10 (23 settembre 2021): 960. http://dx.doi.org/10.3390/ph14100960.

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Abstract (sommario):
The urothelium displays mechano- and chemosensory functions via numerous receptors and channels. The calcium-sensing receptor (CaSR) detects extracellular calcium and modulates several physiological functions. Nonetheless, information about the expression and the role of CaSR in lower urinary tract has been absent. We aimed to determine the existence of urothelial CaSR in urinary bladder and its effect on micturition function. We utilized Western blot to confirm the expression of CaSR in bladder and used immunofluorescence to verify the location of the CaSR in the bladder urothelium via colocalization with uroplakin III A. The activation of urothelial CaSR via the CaSR agonist, AC-265347 (AC), decreased urinary bladder smooth muscle (detrusor) activity, whereas its inhibition via the CaSR antagonist, NPS-2143 hydrochloride (NPS), increased detrusor activity in in vitro myography experiments. Cystometry, bladder nerve activities recording, and bladder surface microcirculation detection were conducted to evaluate the effects of the urothelial CaSR via intravesical administrations. Intravesical AC inhibited micturition reflex, bladder afferent and efferent nerve activities, and reversed cystitis-induced bladder hyperactivity. The urothelial CaSR demonstrated a chemosensory function, and modulated micturition reflex via regulating detrusor activity. This study provided further evidence of how the urothelial CaSR mediated micturition and implicated the urothelial CaSR as a potential pharmacotherapeutic target in the intervention of bladder disorders.
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38

Powell, Charles R., Albert Kim, Joshua Roth, James P. Byrd, Khalid Mohammad, Mouhamad Alloosh, Ragini Vittal e Michael Sturek. "Ossabaw Pig Demonstrates Detrusor Fibrosis and Detrusor Underactivity Associated with Oxidative Stress in Metabolic Syndrome". Comparative Medicine 70, n. 5 (1 ottobre 2020): 329–34. http://dx.doi.org/10.30802/aalas-cm-20-000004.

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Abstract (sommario):
Metabolic Syndrome (MetS) has detrimental effects on the bladder, including detrusor underactivity. The progression and mechanism of disease are poorly understood. A swine model for diabetic bladder dysfunction (DBD) was established because of the pig's human-sized bladder and its ability to develop MetS by dietary modification alone. The hypothesis of this study is that this swine model will demonstrate oxidative stress associated with MetS, which contributes to both bladder fibrosis and detrusor underactivity (DU). Ossabaw pigs underwent dietary modification consisting of a hypercaloric, atherogenic diet for 10 mo to induce MetS, and were compared with a group of control (lean) pigs. Urodynamic studies were performed in both groups to confirm DU. Thiobarbituric acid reactive substances (TBARS) detected in the urine were used to measure oxidative stress activity in the urinary tract, and urinary IL17a was used to detect profibrotic activity. MetS was confirmed by assessing body weight, blood pressure, glucose tolerance, total cholesterol, and triglycerides. The MetS group exhibited an increase in the relative levels of urinary TBARS and IL17a. Bladder pressures at capacity were lower in the MetS group, suggesting DU. Histologic analysis of a cohort of control (lean) and MetS pigs revealed that as compared with the control pigs, the MetS pigs had significantly more collagen in the muscularis layer, but not in the submucosa or mucosa layer. In conclusion, the Ossabaw pig model for diet-induced MetS is associated with oxidative stress and profibrotic activity in the bladder, which results in DU. This has previously been shown in mice and rats, but never in pigs. This novel model will better represent human MetS and DBD because the mechanism and size of the pig bladder more closely resemble that of a human, resulting in a more valid model and facilitating further study into the signaling mechanisms responsible for this impairment.
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39

Alam, Md Naushad, Md Fazal Naser, Kamrun Nahar, Md Waliul Islam, Md Mamunur Rashid, SM Mahbub Alam e Farhana Khatoon. "Association of Detrusor Muscular Activity With the Outcome of Transurethral Resection of Prostate in Patients With Severity of Bladder Outflow Obstruction". Bangladesh Journal of Urology 18, n. 2 (19 settembre 2020): 56–61. http://dx.doi.org/10.3329/bju.v18i2.49277.

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Abstract (sommario):
Objective: To evaluate the association of detrusor muscular activity with outcome of TURP in patients with severity of bladder outflow obstruction. Methods: This is a hospital based cross sectional study conducted in the Department of Urology of Dhaka Medical College Hospital, Dhaka.Elderly male patients having lower urinary tract symptoms (IPSS=20-35) with no retention (non-catheterized patient), who attended in Dhaka Medical College Hospital, were included in the study. A total of 73 patients meeting the enrollment criteria were included in the study. They were evaluated by history, physical examination including DRE and necessary investigations to identify the potential candidates for TURP. Then the potential participants were counseled for Urodynamic study. All patients underwent TURP by expert surgeon. Three months after TURP, repeat Urodynamic study was done and the results were compared to see the outcome. Afterward the data were plotted for the clarification of detrusor contractility at three levels: normal detrusor contractility (voiding pressure 40-60cm of water), detrusor over activity (voiding pressure >60cm of water) and detrusor under activity (voiding pressure <40 cm of water). According to the provisional ICS nomogram for the analysis of voiding, patients were divided into three classes. In BOO Index(PdetQmax-2Qmax),obstructed(BOOI > 40); equivocal(BOOI=20-40);Unobstructed(BOOId” 20) are taken into consideration. The test statistic used to analyze the data was descriptive statistics and ANOVA test. The level of significance was set at 0.05 and P<O.05 was considered significant. Results: Out of 73 patients 8 didn’t attend follow up session and hence excluded keeping 65 for final analysis. The mean age was 66.3 ± 9.7 years (50- 87 years) .Detrusor over activity was present in 13(20%), normal detrusor contractility was observed in 46(70.8%) and weak contractility in 6(9.2%). Peak urinary flow rate was almost similar among patients of different groups. However, voided volume and residual volume were lowest in overactive group and highest in underactive group, while normal group was in between two (p = 0.007 and p = 0.046 respectively). Maximum urinary flow rate and voided urine between patients of moderate and severe bladder outlet obstruction were almost comparable (p =0.120 and p = 0.270 respectively). However, residual urine volume was much higher in the patients of moderate BOO than that in severe BOO (p = 0.001).The patients of OAB experienced a significant improvement in percentage of reduction of residual urine volume compared to normal and underactive bladder (p = 0.002), However, there were no significant difference among the patients with overactive, normal and underactive bladder with respect to peak urinary flow rate and voided urine volume (p = 0.499 and p = 0.847 respectively). Conclusion: TURP is an effective surgical procedure for treatment of BPH, especially for patients with severe degree of BOO with normal or overactive detrusor contraction. Bangladesh Journal of Urology, Vol. 18, No. 2, July 2015 p.56-61
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40

Puri, Basant K., Mussadiq Shah, Peter O. Julu, Michele C. Kingston e Jean A. Monro. "Urinary Bladder Detrusor Dysfunction Symptoms in Lyme Disease". International Neurourology Journal 17, n. 3 (2013): 127. http://dx.doi.org/10.5213/inj.2013.17.3.127.

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41

LANGER, R., R. RON-EL, M. NEWMAN, A. HERMAN e E. CASPI. "Detrusor instability following colposuspension for urinary stress incontinence". BJOG: An International Journal of Obstetrics and Gynaecology 95, n. 6 (giugno 1988): 607–10. http://dx.doi.org/10.1111/j.1471-0528.1988.tb09492.x.

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42

Lowenstein, Lior, Thythy Pham, Shameem Abbasy, Kimberly Kenton, Linda Brubaker, Elizabeth R. Mueller, Susan Shott, Yoram Vardi, Ilan Gruenwald e Mary P. FitzGerald. "Observations relating to urinary sensation during detrusor overactivity". Neurourology and Urodynamics 28, n. 6 (17 dicembre 2008): 497–500. http://dx.doi.org/10.1002/nau.20680.

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43

El Yazami Adli, Oussama, e Jacques Corcos. "Botulinum neurotoxin-A treatment of lower urinary tract symptoms in multiple sclerosis". Canadian Urological Association Journal 8, n. 1-2 (14 gennaio 2014): 61. http://dx.doi.org/10.5489/cuaj.1824.

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Abstract (sommario):
Multiple sclerosis (MS) is the most common neuroinflammatory disease of the central nervous system and a leading cause of disability in young adults. Symptoms related to vesicourethral dysfunction are very prevalent, but not specific to underlying urodynamic abnormalities. Detrusor overactivity and detrusor external sphincter dysynergia are the most frequent findings and are usually linked. Botulinum neurotoxin-A injection represents a significant advance in the management of voiding dysfunction among MS patients failing first-line therapy. It significantly improves patients’ urodynamic parameters and quality of life, with efficacy sustained by repeated injections and minimal risk of adverse events.
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44

Vahabi, Bahareh, Brian A. Parsons, Olena Doran, Anthony Rhodes, Sarah Dean e Marcus J. Drake. "TRPM8 agonists modulate contraction of the pig urinary bladder". Canadian Journal of Physiology and Pharmacology 91, n. 7 (luglio 2013): 503–9. http://dx.doi.org/10.1139/cjpp-2012-0406.

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Abstract (sommario):
The transient receptor potential melastin-8 (TRPM8) channel is activated by the “cooling” compounds menthol and icilin. Pathophysiologically, it is implicated in the overactive bladder and bladder cooling reflex, but the activity of TRPM8 in normal bladder physiology is poorly understood. We investigated the distribution of TRPM8 channels and the effect of TRPM8 agonists on the contractile function of pig bladder (n = 35) strips and whole bladders. The distribution of TRPM8 was examined by immunohistochemistry. The effect of vesical or intravascular menthol (0.1–0.3 mmol/L) or icilin (50 μmol/L) on carbachol-induced isolated whole bladder contractions was monitored by recording vesical pressure. Strips of denuded detrusor or mucosa were mounted in organ baths to study the effect of TRPM8 agonists on the contractile responses to 10 μmol/L carbachol. TRPM8-like immunoreactivity was detected on pig urothelium. Intravascular menthol (0.3 mmol/L) and icilin (50 μmol/L) significantly decreased the magnitude of carbachol-induced whole bladder contraction, whereas vesical administration significantly increased the response. In detrusor and mucosal strips, both menthol (0.3 mmol/L) and icilin (50 μmol/L) inhibited carbachol-induced contractions. We conclude that the TRPM8 channel is expressed on the urothelium of pig bladder. In the whole organ, exposure of the urothelium to menthol or icilin increases the contractile response to carbachol. Where detrusor muscle is exposed directly to these compounds, the contractile response to carbachol is reduced.
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45

Campos-Sousa, Raimundo Nonato, Elizabeth Maria Aparecida Barasnevicius Quagliato, Kelson James Almeida, Inacio Augusto Dias de Castro e Viriato Campelo. "Urinary dysfunction with detrusor hyperactivity in women with Parkinson's disease cannot be blamed as a factor of worsening motor performance". Arquivos de Neuro-Psiquiatria 71, n. 9A (settembre 2013): 591–95. http://dx.doi.org/10.1590/0004-282x20130101.

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Abstract (sommario):
Introduction Detrusor hyperactivity is the leading cause of urinary dysfunction in Parkinson's disease (PD). There are few studies correlating PD clinical aspects with this autonomic feature. Methods A cohort of 63 women with PD were prospectively examined for assessment of clinical aspects and disease severity using unified Parkinson's disease rating scale and Hoehn-Yahr scale, respectively. The urologic function was evaluated by the urodynamic study. Two groups were categorized at this time - groups with and without detrusor hyperactivity. After seven years, the same parameters were re-evaluated. Results Progression of the disease on mental scores was found in the group with detrusor hyperactivity. On follow-up, clinical symptoms and severity did not show significant worsening between the groups. Conclusion Detrusor hyperactivity is a frequent urodynamic finding in PD, and even though it is associated with dopaminergic dysfunction, it cannot be blamed as a factor of worsening motor performance, but is probably associated with poor cognitive and mental prognosis.
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46

Macnab, Andrew J., Lynn S. Stothers e Babak Shadgan. "Monitoring Detrusor Oxygenation and Hemodynamics Noninvasively during Dysfunctional Voiding". Advances in Urology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/676303.

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Abstract (sommario):
The current literature indicates that lower urinary tract symptoms (LUTSs) related to benign prostatic hyperplasia (BPH) have a heterogeneous pathophysiology. Pressure flow studies (UDSs) remain the gold standard evaluation methodology for such patients. However, as the function of the detrusor muscle depends on its vasculature and perfusion, the underlying causes of LUTS likely include abnormalities of detrusor oxygenation and hemodynamics, and available treatment options include agents thought to act on the detrusor smooth muscle and/or vasculature. Hence, near infrared spectroscopy (NIRS), an established optical methodology for monitoring changes in tissue oxygenation and hemodynamics, has relevance as a means of expanding knowledge related to the pathophysiology of BPH and potential treatment options. This methodological report describes how to conduct simultaneous NIRS monitoring of detrusor oxygenation and hemodynamics during UDS, outlines the clinical implications and practical applications of NIRS, explains the principles of physiologic interpretation of NIRS voiding data, and proposes an exploratory hypothesis that the pathophysiological causes underlying LUTS include detrusor dysfunction due to an abnormal hemodynamic response or the onset of oxygen debt during voiding.
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47

Lin, Yu-Hua, Bing-Juin Chiang e Chun-Hou Liao. "Mechanism of Action of Botulinum Toxin A in Treatment of Functional Urological Disorders". Toxins 12, n. 2 (18 febbraio 2020): 129. http://dx.doi.org/10.3390/toxins12020129.

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Abstract (sommario):
Intravesical botulinum toxin (BoNT) injection is effective in reducing urgency and urinary incontinence. It temporarily inhibits the detrusor muscle contraction by blocking the release of acetylcholine (Ach) from the preganglionic and postganglionic nerves in the efferent nerves. BoNT-A also blocks ATP release from purinergic efferent nerves in the detrusor muscle. In afferent nerves, BoNT-A injection markedly reduces the urothelial ATP release and increases nitric oxide (NO) release from the urothelium. BoNT-A injection in the urethra or bladder has been developed in the past few decades as the treatment method for detrusor sphincter dyssyndergia, incontinence due to neurogenic or idiopathic detrusor overactivity, sensory disorders, including bladder hypersensitivity, overactive bladder, and interstitial cystitis/chronic pelvic pain syndrome. Although the FDA only approved BoNT-A injection treatment for neurogenic detrusor overactivity and for refractory overactive bladder, emerging clinical trials have demonstrated the benefits of BoNT-A treatment in functional urological disorders. Cautious selection of patients and urodynamic evaluation for confirmation of diagnosis are crucial to maximize the successful outcomes of BoNT-A treatment.
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48

Silva, Isabel, Ana Filipa Costa, Sílvia Moreira, Fátima Ferreirinha, Maria Teresa Magalhães-Cardoso, Isabel Calejo, Miguel Silva-Ramos e Paulo Correia-de-Sá. "Inhibition of cholinergic neurotransmission by β3-adrenoceptors depends on adenosine release and A1-receptor activation in human and rat urinary bladders". American Journal of Physiology-Renal Physiology 313, n. 2 (1 agosto 2017): F388—F403. http://dx.doi.org/10.1152/ajprenal.00392.2016.

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Abstract (sommario):
The direct detrusor relaxant effect of β3-adrenoceptor agonists as a primary mechanism to improve overactive bladder symptoms has been questioned. Among other targets, activation of β3-adrenoceptors downmodulate nerve-evoked acetylcholine (ACh) release, but there is insufficient evidence for the presence of these receptors on bladder cholinergic nerve terminals. Our hypothesis is that adenosine formed from the catabolism of cyclic AMP in the detrusor may act as a retrograde messenger via prejunctional A1 receptors to explain inhibition of cholinergic activity by β3-adrenoceptors. Isoprenaline (1 µM) decreased [3H]ACh release from stimulated (10 Hz, 200 pulses) human (−47 ± 5%) and rat (−38 ± 1%) detrusor strips. Mirabegron (0.1 µM, −53 ± 8%) and CL316,243 (1 µM, −37 ± 7%) mimicked isoprenaline (1 µM) inhibition, and their effects were prevented by blocking β3-adrenoceptors with L748,337 (30 nM) and SR59230A (100 nM), respectively, in human and rat detrusor. Mirabegron and isoprenaline increased extracellular adenosine in the detrusor. Blockage of A1 receptors with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 100 nM) or the equilibrative nucleoside transporters (ENT) with dipyridamole (0.5 µM) prevented mirabegron and isoprenaline inhibitory effects. Dipyridamole prevented isoprenaline-induced adenosine outflow from the rat detrusor, and this effect was mimicked by the ENT1 inhibitor, S-(4-nitrobenzyl)-6-thioinosine (NBTI, 30 µM). Cystometry recordings in anesthetized rats demonstrated that SR59230A, DPCPX, dipyridamole, and NBTI reversed the decrease in the voiding frequency caused by isoprenaline (0.1–1,000 nM). Data suggest that inhibition of cholinergic neurotransmission by β3-adrenoceptors results from adenosine release via equilibrative nucleoside transporters and prejunctional A1-receptor stimulation in human and rat urinary bladder.
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49

Smith, Phillip P., Anthony DeAngelis e George A. Kuchel. "Detrusor expulsive strength is preserved, but responsiveness to bladder filling and urinary sensitivity is diminished in the aging mouse". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, n. 5 (1 marzo 2012): R577—R586. http://dx.doi.org/10.1152/ajpregu.00508.2011.

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Abstract (sommario):
The prevalence of urinary symptoms increases with age and is a significant source of distress, morbidity, and expense in the elderly. Recent evidence suggests that symptoms in the aged may result from sensory dysfunction, rather than abnormalities of detrusor performance. Therefore, we employed a pressure/flow multichannel urethane-anesthetized mouse cystometry model to test the hypothesis that in vivo detrusor performance does not degrade with aging. Secondarily, we sought to evaluate sensory responsiveness to volume using pressure-volume data generated during bladder filling. Cystometric data from 2-, 12-, 22-, and 26-mo-old female C57BL6 mice were compared. All 2- and 12-mo-old mice, 66% of 22-mo-old mice, and 50% of 26-mo-old mice responded to continuous bladder filling with periodic reflex voiding. Abdominal wall contraction with voiding had a minimal contribution to expulsive pressure, whereas compliance pressure was a significant contributor. Maximum bladder pressure, estimated detrusor pressure, detrusor impulse (pressure-time integral), as well as indices of detrusor power and work, did not decrease with aging. Bladder precontraction pressures decreased, compliance increased, and nonvoiding contraction counts did not change with increasing age. Intervoid intervals, per-void volumes, and voiding flow rates increased with age. Calculations approximating wall stress during filling suggested loss of bladder volume sensitivity with increasing age. We conclude that aging is associated with an impaired ability to respond to the challenge of continuous bladder filling with cyclic voiding, yet among responsive animals, voiding detrusor contraction strength does not degrade with aging in this murine model. Furthermore, indirect measures suggest that bladder volume sensitivity is diminished. Thus, changes in homeostatic reserve and peripheral and/or central sensory mechanisms may be important contributors to aging-associated changes in bladder function.
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50

Southern, Jordan B., Jasmine R. Frazier, Amy S. Miner, John E. Speich, Adam P. Klausner e Paul H. Ratz. "Elevated steady-state bladder preload activates myosin phosphorylation: detrusor smooth muscle is a preload tension sensor". American Journal of Physiology-Renal Physiology 303, n. 11 (1 dicembre 2012): F1517—F1526. http://dx.doi.org/10.1152/ajprenal.00278.2012.

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Abstract (sommario):
In rabbit bladder wall (detrusor) muscle, the degree of tone induced during physiological filling (filling tone) is the sum of adjustable preload tension and autonomous contractile tension. The present study was designed to determine whether the level of filling tone is dependent on detrusor muscle length. Maximum active tension induced by KCl was parabolic in relation to length [tension increased from 70% to 100% of a reference length ( Lref) and decreased at longer muscle lengths]. Filling tone, however, increased in a linear fashion from 70% to 120% Lref. In the presence of ibuprofen to abolish autonomous contraction and retain adjustable preload tension, tension was reduced in strength but remained linearly dependent on length from 70% to 120% Lref. In the absence of autonomous contraction, stretching detrusor muscle from 80% to 120% Lref still caused an increase in tone during PGE2-induced rhythmic contraction, suggesting that muscle stretch caused increases in detrusor muscle contractile sensitivity rather than in prostaglandin release. In the absence of autonomous contraction, the degree of adjustable preload tension and myosin phosphorylation increased when detrusor was stretched from 80% to 120% Lref, but also displayed length-hysteresis, indicating that detrusor muscle senses preload rather than muscle length. Together, these data support the hypothesis that detrusor muscle acts as a preload tension sensor. Because detrusor muscle is in-series with neuronal mechanosensors responsible for urinary urgency, a more thorough understanding of detrusor muscle filling tone may reveal unique targets for therapeutic intervention of contractile disorders such as overactive bladder.
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