ArticleMolecular and cellular biochemistry1999
Metabolic basis for contractile dysfunction following chronic partial bladder outlet obstruction in rabbits.
Article in Molecular and cellular biochemistry, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 27 citations in OpenAlex.
- Detrusor underactivity: Pathophysiological considerations, models and proposals for future research. ICI-RS 2013.Neurourology and urodynamics · 2014Article
- Protective action of intravesical oxybutynin on bladder ultrastructure in rabbits with detrusor overactivity.International urogynecology journal and pelvic floor dysfunction · 2009Article
- Mechanistic insights into the role of alpha1adrenergic receptors in lower urinary tract symptoms.Current urology reports · 2004Review
- Vascular response of the rabbit bladder to chronic partial outlet obstruction.Molecular and cellular biochemistry · 2001Article
- Vascular response of the rabbit bladder to short term partial outlet obstruction.Molecular and cellular biochemistry · 2000Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prior studies have shown that partial outlet obstruction of the rabbit bladder causes a progressive increase in bladder mass, a progressive decrease in the contractile response to different forms of stimulation, and a selective decrease in the activity of mitochondrial enzymes. In this investigation the contractile responses to field stimulation and bethanechol were directly correlated with the activity of citrate synthase as a function of both the duration of obstruction and the bladder mass. Partial bladder outlet obstruction was surgically induced in twenty New Zealand White rabbits. The bladders were then rapidly excised at 30, 40, 90, 105 or 150 days post obstruction. The contractile responses to field stimulation (32 Hz) and bethanechol (250 microM) were determined. The remainder of the bladders were frozen and used for citrate synthase activity determinations. The data were grouped for analysis both by the duration of obstruction and by the bladder mass. Chronic partial outlet obstruction caused a parallel decline in the activity of citrate synthase and in the response of the obstructed tissue to stimulation.
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