Radiotelemetered urodynamics of obstructed ovine fetal bladders: correlations with <i>ex vivo</i> cystometry and renal histopathology

Farrugia, Marie Klaire; Woolf, Adrian S.; Fry, Christopher; Peebles, Donald; Cuckow, Peter; Godley, Margaret L.

doi:10.1111/j.1464-410x.2007.06799.x

Cited by 9 publications

(7 citation statements)

References 16 publications

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“…E, Statistical analyses of urodynamic parameters obtained from the PV loop. No statistical difference is evident between the mean values of the parameters measured during the first (0-10) and the second (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) or the last (20-30) 10 minutes of the recording period. Apv, the area enclosed by a loop trajectory (NS, no significance vs 0-10, all n = 7)…”

Section: Altered Preloadsmentioning

confidence: 88%

Pressure‐volume analysis of rat's micturition cycles in vivo

Peng

Lai

Hsieh

et al. 2020

Neurourology and Urodynamics

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Aims Though the pressure‐volume analysis (PVA), a method based on thermodynamics, is broadly used for assaying cardiac functions, its potential application on the physiology/pathophysiology of the urinary bladder, which processes resemble thermodynamic cycles to the heart, has not been established. Methods Cystometry recording intravesical pressure (IVP) and intravesical volume (IVV) of rhythmic voiding contractions caused by a constant saline infusion (0.04 mL/min) were carried out in forty urethane‐anesthetized female Sprague‐Dawley rats, and the PVA was established by plotting IVP against IVV. Results Pressure‐volume points shaped coincident enclosed loops, and loop‐associated urodynamic parameters kept stable under a constant infusion rate (0.04 mL/min). Enhancing preload (by elevating infusion rates to 0.08 and 0.12 mL/min) increased the area enclosed by the loop (Apv) and shifted loops to the right and slightly upward. Augmenting afterload (by enhancing resistances using 1/4 and 1/2 urethra clamping) increased Apv and shifted loops markedly to the right and upward. Without affecting Apv, muscarine (0.01 and 0.1 mM)‐induced inotropic states shifted loop to the left and upward that was as opposed to the atropine (0.01 and 0.1 mM)‐induced anti‐inotropic state. Conclusions Not only consistently assayed baseline bladder functions, PVA but also validly measured modified bladder functions due to altered extrinsic environment and intrinsic contractility of the bladder itself. In accompanied by cystometry, PVA could provide a clear concept about the relationship between time, pressure, and volume in the voiding activity.

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Section: Altered Preloadsmentioning

confidence: 88%

Pressure‐volume analysis of rat's micturition cycles in vivo

Peng

Lai

Hsieh

et al. 2020

Neurourology and Urodynamics

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“…Healthy human bladders also undergo cyclical filling and voiding before birth [ 28 ]. Furthermore, ligating the urethra in foetal sheep leads to persistently and markedly raised intravesical pressures [ 29 ]. Foetal ultrasonographic anomaly screening of individuals who are later diagnosed as having UFS can show megacystis, or a grossly dilated bladder, and/or dilated ureters [ 25 , 27 ].…”

Section: Ufs Bladders Fail To Undergo Functional Differentiamentioning

confidence: 99%

From gene discovery to new biological mechanisms: heparanases and congenital urinary bladder disease

Roberts

Hilton

Woolf

2015

Nephrol. Dial. Transplant.

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We present a scientific investigation into the pathogenesis of a urinary bladder disease. The disease in question is called urofacial syndrome (UFS), a congenital condition inherited in an autosomal recessive manner. UFS features incomplete urinary bladder emptying and vesicoureteric reflux, with a high risk of recurrent urosepsis and end-stage renal disease. The story starts from a human genomic perspective, then proceeds through experiments that seek to determine the roles of the implicated molecules in embryonic frogs and newborn mice. A future aim would be to use such biological knowledge to intelligently choose novel therapies for UFS. We focus on heparanase proteins and the peripheral nervous system, molecules and tissues that appear to be key players in the pathogenesis of UFS and therefore must also be critical for functional differentiation of healthy bladders. These considerations allow the envisioning of novel biological treatments, although the potential difficulties of targeting the developing bladder in vivo should not be underestimated.

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“…Severe forms cause oligohydramnios and are associated with dysplastic kidney malformations that can be secondary to LUTO 11 . This can be deduced because similar kidney disease occurs in ovine fetuses with surgically generated LUTO 12 . Indeed, LUTOs are the leading cause for end-stage renal disease (ESRD) in children 13 .…”

Section: Main Textmentioning

confidence: 99%

Rare Variants in BNC2 Are Implicated in Autosomal-Dominant Congenital Lower Urinary-Tract Obstruction

Kolvenbach

Dworschak

Frese

et al. 2019

The American Journal of Human Genetics

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Congenital lower urinary-tract obstruction (LUTO) is caused by anatomical blockage of the bladder outflow tract or by functional impairment of urinary voiding. About three out of 10,000 pregnancies are affected. Although several monogenic causes of functional obstruction have been defined, it is unknown whether congenital LUTO caused by anatomical blockage has a monogenic cause. Exome sequencing in a family with four affected individuals with anatomical blockage of the urethra identified a rare nonsense variant (c.2557C>T [p.Arg853∗]) in BNC2, encoding basonuclin 2, tracking with LUTO over three generations. Re-sequencing BNC2 in 697 individuals with LUTO revealed three further independent missense variants in three unrelated families. In human and mouse embryogenesis, basonuclin 2 was detected in lower urinary-tract rudiments. In zebrafish embryos, bnc2 was expressed in the pronephric duct and cloaca, analogs of the mammalian lower urinary tract. Experimental knockdown of Bnc2 in zebrafish caused pronephric-outlet obstruction and cloacal dilatation, phenocopying human congenital LUTO. Collectively, these results support the conclusion that variants in BNC2 are strongly implicated in LUTO etiology as a result of anatomical blockage.

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Radiotelemetered urodynamics of obstructed ovine fetal bladders: correlations with ex vivo cystometry and renal histopathology

Cited by 9 publications

References 16 publications

Pressure‐volume analysis of rat's micturition cycles in vivo

Pressure‐volume analysis of rat's micturition cycles in vivo

From gene discovery to new biological mechanisms: heparanases and congenital urinary bladder disease

Rare Variants in BNC2 Are Implicated in Autosomal-Dominant Congenital Lower Urinary-Tract Obstruction

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