Alterations in cholinergic and neuropeptide innervation of urinary bladder following partial bladder outlet obstruction (original) (raw)

Neuroanatomical changes in the rat bladder after bladder outlet obstruction

BJU International, 1998

Objective To investigate the histological changes in blad-alterations in bladder capacity and voided pressures; obstructed animals had markedly increased bladder der innervation in response to partial bladder outlet obstruction in a rat model. capacities and higher voiding pressures (obstructed, 80-100 cmH 2 O; normal, 30-40 cmH 2 O). Neuronal Materials and methods Forty-eight adult female rats had their bladder outlet partially obstructed by ligating the changes in the obstructed bladder were most dramatic within the cholinergic and adrenergic neuro-proximal urethra over a 20 G angiocatheter; 18 shamoperated rats served as controls. Animals were transmitter systems within and surrounding the smooth muscle bundles, where there was less staining killed after 1, 2 and 4 weeks, and their bladders evaluated using computerized morphometry. than in control animals. PGP immunoreactivity increased slightly. The l-arginine-nitric oxide pathway Immunohistochemical staining for neuronal protein gene-product 9.5 (PGP, a general neuronal marker) appeared unperturbed after obstruction. Conclusions These histological findings suggest that and enzyme histochemical staining of acetylcholinesterase, adrenergic fibres and nitric oxide synthase were neuropathic changes in the bladder after outlet obstruction, including detrusor instability, are mainly performed. Results Bladder wall changes after obstruction consisted the result of anatomical perturbations in the cholinergic and adrenergic pathways. of a six-to sevenfold increase in bladder volume and weight. Smooth muscle hypertrophy was evident equ-Keywords Bladder, smooth muscle hypertrophy, neuronal changes ally at all sample times. Cystometry showed functional neurotransmitters within the bladder has generated

Effect of Bladder Outflow Obstruction on the Innervation of the Rabbit Urinary Bladder

British Journal of Urology, 1990

The effects of bladder outflow obstruction on the innervation of the bladder were studied using a rabbit animal model. Partial occlusion of the bladder neck was obtained by the placement of a silk ligature at that level; control animals underwent a sham procedure. After a 3month period, the presence of outflow tract obstruction was confirmed using urodynamic studies.

Effect of short-term outlet obstruction on rat bladder nerve density and contractility

Autonomic & Autacoid Pharmacology, 2007

1 The present study was designed to investigate the relationship between innervation density and contractile responses to field stimulation and exogenous agonists at early time points after induction of bladder outlet obstruction (BOO) in rats. 2 When compared with sham-operated animals, 1, 3 and 7 days of BOO were associated with a 75%, 80% and 90% increase of bladder weight. Field stimulation caused a frequencydependent increase in force of contraction. The force of contraction was reduced at each frequency in BOO rats with the greatest decrease after 1 day and a gradual but incomplete recovery thereafter. In contrast, contractile responses to ATP, carbachol and KCl were markedly reduced after 1 day of BOO and fully recovered after 7 days. The neurofilament staining was not altered by 1 day of BOO, but gradually decreased with increasing duration of BOO reaching the lowest levels after 7 days. 3 We conclude that impaired cellular contractility seems to underlie the early reductions of field stimulation-induced contraction, possibly reflecting surgical trauma of the tissue. However, at later time points a reduced nerve density, possibly reflecting a partial denervation, appears to be the main reason for impaired contractile response to field stimulation.

Damage to the bladder neck alters autonomous activity and its sensitivity to cholinergic agonists

BJU International, 2007

Adult male guinea pigs (294-454 g) were assigned initially into three groups: (i) normal guinea pigs with no surgical intervention (control, seven); (ii) guinea pigs which, with full surgical anaesthesia, had a silver ring implanted around the bladder neck (obstructed, 13); and (iii) guinea pigs operated to expose the bladder neck but with no implantation of a ring (sham, six). At 2-4 weeks after surgery the bladders were isolated, weighed and the pressure recordings used to identify autonomous activity.

Peripheral modulation of bladder activity : sensory and motor

2017

Front cover image: Created by Prof. dr. James Gillespie Record of arecaidine-induced autonomous bladder activity in an isolated guinea pig bladder. Immunohistochemistry picture of the major pelvic ganglion of the rat: sensory nerves staining for calcitonin gene-related peptide synapsing with small intensely fluorescent cells immunoreactive for the β 3-adrenoceptor. Cartoon illustrating the neural circuits in the major pelvic ganglion.

Bladder afferents and their role in the overactive bladder* 1

Urology, 2002

The role of afferent innervation of the bladder in the pathophysiology of urinary incontinence has become the focus of intense interest. In normal health, the afferent pathway is mediated largely by A␦-fibers, which ultimately send information about the state of bladder fullness to the pontine micturition center via the periaqueductal gray matter. However, after spinal disruption, a different type of afferent pathway emerges, mediated by capsaicin-sensitive C-fibers that drive a spinal segmental reflex pathway, causing neurogenic detrusor overactivity. The common sources of afferent information for either pathway are likely to be afferents from the urothelium, lamina propria, and afferents that originate in the bladder wall. Ultrastructural investigations of the constituent neural elements of these structures contribute to our knowledge of their role in both health and disease and help provide a rational approach to treatment strategies. Evidence of the involvement of capsaicin-sensitive C-fibers in the spinal reflex pathway has been supported by the successful treatment of patients with neurogenic incontinence with intravesical capsaicin or its ultrapotent nonpungent analog, resiniferatoxin. On the other hand, capsaicin has not been shown to be clearly effective in treatment of overactive bladder caused by detrusor overactivity or suprapontine pathology without the emergent C-fiber-mediated reflex. It is hoped that continued investigation of neurotoxins that have the potential to act on afferent innervation will lead to other treatment strategies for bladder disorders and other disorders involving afferent dysfunction. UROLOGY 59 (Suppl 5A): 37-42, 2002. © 2002,