Br J Urol 1998 Dec;82(6):895-901

Urology Service, Tripler Army Medical Center, Hawaii.

Objective: To investigate the histological changes in bladder innervation in response to partial bladder outlet obstruction in a rat model.

Materials And Methods: Forty-eight adult female rats had their bladder outlet partially obstructed by ligating the proximal urethra over a 20 G angiocatheter; 18 shamoperated rats served as controls. Animals were killed after 1, 2 and 4 weeks, and their bladders evaluated using computerized morphometry. Immunohistochemical staining for neuronal protein gene-product 9.5 (PGP, a general neuronal marker) and enzyme histochemical staining of acetylcholinesterase, adrenergic fibres and nitric oxide synthase were performed.

Results: Bladder wall changes after obstruction consisted of a six- to sevenfold increase in bladder volume and weight. Smooth muscle hypertrophy was evident equally at all sample times. Cystometry showed functional alterations in bladder capacity and voided pressures; obstructed animals had markedly increased bladder capacities and higher voiding pressures (obstructed, 80-100 cmH2O; normal, 30-40 cmH2O). Neuronal changes in the obstructed bladder were most dramatic within the cholinergic and adrenergic neurotransmitter systems within and surrounding the smooth muscle bundles, where there was less staining than in control animals. PGP immunoreactivity increased slightly. The L-arginine-nitric oxide pathway appeared unperturbed after obstruction.

Conclusions: These histological findings suggest that neuropathic changes in the bladder after outlet obstruction, including detrusor instability, are mainly the result of anatomical perturbations in the cholinergic and adrenergic pathways.
December 1998
7 Reads

Publication Analysis

Top Keywords

bladder outlet
outlet obstruction
cholinergic adrenergic
smooth muscle
changes bladder
pressures obstructed
bladder wall
wall changes
changes obstruction
protein gene-product
control animals
animals pgp
synthase performedresults
performedresults bladder
staining control
obstruction consisted
neuronal protein
sevenfold increase
increase bladder

Similar Publications

Acute increase in blood flow to the rat bladder subsequent to partial bladder outlet obstruction.

Neurourol Urodyn 2000 ;19(2):195-206; discussion 206-8

Department of Urology, The College of Physicians and Surgeons of Columbia University, New York, New York, USA.

Partial obstruction of the rat bladder outlet initiates a multi-step process during which the bladder progressively loses its functional ability. The first step in this progression is bladder hypertrophy; the organ dramatically increases in size and weight to compensate for the effects of obstruction. Unoperated female rats, age-matched, sham-obstructed rats, and rats that received a partial bladder outlet obstruction were studied. Read More

View Article
April 2000

Change in acetylcholine release from rat bladder with partial outlet obstruction.

BJU Int 2008 Mar 7;101(5):633-9. Epub 2007 Dec 7.

Department of Urology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Objective: To investigate changes in acetylcholine release from the bladder of rats with partial bladder outlet obstruction (BOO), as partial BOO leads to hypertrophy and an alteration in the contractions of the detrusor smooth muscle, and acetylcholine plays an important role in urinary bladder contractions but there is little available information on acetylcholine release after BOO.

Material And Methods: Partial BOO was induced in adult female rats by ligating the proximal urethra over a 1 mm angiocatheter; sham-operated rats served as controls. The rats were killed 2 weeks, 3 and 6 months after induction of BOO. Read More

View Article
March 2008

Altered response to partial bladder outlet obstruction in mice lacking inducible nitric oxide synthase.

J Urol 2000 Jun;163(6):1981-7

Department of Urology, University of Texas - Southwestern Medical Center, Dallas, Texas, USA.

Introduction: Following prolonged partial bladder outlet obstruction (BOO) in the mouse, cholinergic mediated detrusor contractility decreases. Previous work has demonstrated an increase in the inducible form of nitric oxide synthase (iNOS) at the mRNA and protein levels soon after obstruction. Since nitric oxide (NO), the product of the action of iNOS on molecular oxygen and l-arginine, produces vasodilation and decreases platelet aggregation, we believe it is an integral part of the initial detrusor response to obstruction. Read More

View Article
June 2000

Effects of chronic partial outlet obstruction on blood flow and oxygenation of the rat bladder.

J Urol 2002 Mar;167(3):1508-12

Department of Urology, College of Physicians and Surgeons of Columbia University, New York , USA.

Purpose: Experimental partial bladder outlet obstruction in rats and rabbits drives the bladder through 3 sequential responses, referred to as hypertrophy, compensation and decompensation. The hypertrophy phase, which is a period of rapid bladder growth, has previously been shown to be accompanied by a significant increase in bladder blood flow in rats and rabbits in a manner that likely supports the bladder cell growth process. However, chronic periods of obstruction in the rabbit have been shown to reduce significantly bladder blood flow, especially to the detrusor smooth muscle, corresponding with a loss of bladder contractile function or decompensation in these animals. Read More

View Article
March 2002