Key result
cAMP-dependent inotropes produce weaker maximal contractility than calcium or ouabain in diseased human myocardium.
Why the study?
The maximal positive inotropic effects of various compounds acting through cyclic adenosine monophosphate in diseased human ventricular myocardium were unclear compared to ouabain.
Do cAMP-mediated inotropic substances increase force of contraction compared to or additively with ouabain in isolated diseased human ventricular myocardium?
Population
Isolated contracting human ventricular myocardium from patients undergoing mitral valve replacement
Comparison
Positive inotropic compounds versus maximal ouabain effect
Design
Preclinical experimental study
Authors
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May limit cAMP inotrope use in heart failure; leaves open additive benefit with ouabain in clinical settings.
Do cAMP-mediated inotropic substances increase force of contraction compared to or additively with ouabain in isolated diseased human ventricular myocardium?
Inotropic agents acting via cAMP yield submaximal responses in diseased human myocardium and increase toxicity without added benefit when combined with maximal ouabain.
Brown et al. (1986) studied Diseased human ventricular myocardium. Positive inotropic substances (cAMP-dependent) vs. Calcium and ouabain was evaluated on Force of contraction. Inotropic substances acting through cyclic AMP produced significantly lower maximal inotropic responses than calcium or ouabain in isolated diseased human ventricular myocardium.
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