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Endocardial function in pacing-induced heart failure in the dog
K Li1, J L Rouleau, A Calderone
1Department of Medicine, Université de Sherbrooke, Québec, Canada.
Journal of Molecular and Cellular Cardiology
|May 1, 1993
Summary
The endocardial endothelium in heart failure modulates myocardial contractility and alpha-1-adrenergic responsiveness. This study shows endocardial endothelium dysfunction contributes to decreased alpha-1-adrenergic responsiveness in a canine pacing-overdrive heart failure model.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Heart Failure Pathophysiology
Background:
- The endocardial endothelium influences myocardial contractility and adrenergic responsiveness.
- Heart failure models exhibit altered contractile function and adrenergic signaling.
Purpose of the Study:
- To investigate the role of the endocardial endothelium in modulating myocardial contractility and alpha-1-adrenergic responsiveness in a canine pacing-overdrive heart failure model.
- To determine if endocardial endothelial dysfunction contributes to altered adrenergic responsiveness in heart failure.
Main Methods:
- Utilized a canine pacing-overdrive model to induce heart failure.
- Isolated papillary muscles were used to assess contractile characteristics (total tension, time to 1/2 tension decline).
- Alpha-1-adrenergic responsiveness was evaluated using phenylephrine concentration-response curves before and after endocardial endothelial removal.
Main Results:
- Pacing-overdrive heart failure significantly decreased total tension and altered twitch kinetics.
- Endocardial endothelial removal in control muscles caused modest decreases in tension and altered kinetics.
- In pacing-overdrive muscles, endocardial endothelial removal further reduced tension and altered kinetics, indicating continued modulation.
- Alpha-1-adrenergic responsiveness was blunted in pacing-overdrive muscles, and endocardial endothelial removal did not further shift the phenylephrine concentration-response curve, suggesting endothelium-dependent dysfunction.
Conclusions:
- The endocardial endothelium directly modulates myocardial contractile characteristics independently of circulating plasma substances.
- Endocardial endothelium dysfunction is a key factor contributing to the decreased alpha-1-adrenergic responsiveness observed in this heart failure model.
- These findings highlight the critical role of endocardial endothelial integrity in maintaining normal cardiac function during heart failure.