Key result
Digoxin administration for 1 week in rabbits with heart failure significantly attenuated the down-regulation of myocardial beta-adrenergic receptors compared to saline (39.9 vs 28.8 fmol/mg protein, p<0.05).
Why the study?
Does digoxin improve beta-adrenergic sympathetic activities and hemodynamics in a rabbit model of heart failure?
Population
22 Japanese white rabbits with heart failure induced by aortic regurgitation (n=14) or sham operation (n=8)
Comparison
Digoxin for 1 week vs Saline for 1 week or sham operation
Design
Preclinical
Follow-up
1 week
Authors
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May guide preclinical digoxin research on beta-receptors; leaves open translation to human heart failure therapy.
Does digoxin improve beta-adrenergic sympathetic activities and hemodynamics in a rabbit model of heart failure?
Absolute Event Rate: 39.9% vs 28.8%
p-value: p=<0.05
In a rabbit model of heart failure, chronic digoxin treatment improved hemodynamic variables and partially restored myocardial beta-adrenergic receptor numbers.
ALBAJINAI et al. (1997) studied Heart failure (aortic regurgitation) (n=22). Digoxin vs. Saline was evaluated on Myocardial beta-adrenergic receptor density (p=<0.05). Digoxin administration for 1 week in rabbits with heart failure significantly attenuated the down-regulation of myocardial beta-adrenergic receptors compared to saline (39.9 vs 28.8 fmol/mg protein, p<0.05).
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