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Research Article Free access | 10.1172/JCI119101

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

G E Newton, A B Parker, J S Landzberg, W S Colucci, and J D Parker

Cardiovascular Division, Department of Medicine, Mount Sinai Hospital, the University of Toronto, Ontario, Canada.

Find articles by Newton, G. in: PubMed | Google Scholar

Cardiovascular Division, Department of Medicine, Mount Sinai Hospital, the University of Toronto, Ontario, Canada.

Find articles by Parker, A. in: PubMed | Google Scholar

Cardiovascular Division, Department of Medicine, Mount Sinai Hospital, the University of Toronto, Ontario, Canada.

Find articles by Landzberg, J. in: PubMed | Google Scholar

Cardiovascular Division, Department of Medicine, Mount Sinai Hospital, the University of Toronto, Ontario, Canada.

Find articles by Colucci, W. in: PubMed | Google Scholar

Cardiovascular Division, Department of Medicine, Mount Sinai Hospital, the University of Toronto, Ontario, Canada.

Find articles by Parker, J. in: PubMed | Google Scholar

Published December 15, 1996 - More info

Published in Volume 98, Issue 12 on December 15, 1996
J Clin Invest. 1996;98(12):2756–2763. https://doi.org/10.1172/JCI119101.
© 1996 The American Society for Clinical Investigation
Published December 15, 1996 - Version history
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Abstract

The objective of this study was to evaluate the effect of muscarinic receptor modulation on basal and beta-adrenergic stimulated left ventricular function in patients with heart failure. 21 heart failure patients and 14 subjects with normal ventricular function were studied. In Protocol 1 intracoronary acetylcholine resulted in a 60+/-8% inhibition of the left ventricular +dP/dt response to intracoronary dobutamine in the normal group, and a similar 70+/-13% inhibition in the heart failure group. Acetylcholine also attenuated the dobutamine-mediated acceleration of isovolumic relaxation (Tau) in both groups. Acetylcholine alone had no effect on Tau in the normal group, while it prolonged Tau in the heart failure group. In Protocol 2 intracoronary atropine resulted in a 35+/-10% augmentation of the inotropic response to dobutamine in the normal group, versus a non-significant 12+/-15% augmentation of the dobutamine response in the heart failure group. In Protocol 3, in 6 heart failure patients, both effects of acetylcholine, the slowing of ventricular relaxation and the inhibition of beta-adrenergic responses, were reversed by the addition of atropine. Therefore, in the failing human left ventricle muscarinic stimulation has an independent negative lusitropic effect and antagonizes the effects of beta-adrenergic stimulation.

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