Inotropic and lusitropic dysfunction in myocardium from patients with dilated cardiomyopathy
- 1 January 1992
- journal article
- Published by Elsevier in American Heart Journal
- Vol. 123 (1), 116-128
- https://doi.org/10.1016/0002-8703(92)90755-k
Abstract
No abstract availableKeywords
This publication has 42 references indexed in Scilit:
- Increase of Gi alpha in human hearts with dilated but not ischemic cardiomyopathy.Circulation, 1990
- Effectiveness of Cardiac Glycosides in Human Myocardium With and Without “Downregulated” β-AdrenoceptorsJournal of Cardiovascular Pharmacology, 1990
- Basal and Isoprenaline-Stimulated cAMP Content in Failing Versus Nonfailing Human Cardiac PreparationsJournal of Cardiovascular Pharmacology, 1989
- INCREASE IN MYOCARDIAL Gi-PROTEINS IN HEART FAILUREThe Lancet, 1988
- Increase of the 40,000-mol wt pertussis toxin substrate (G protein) in the failing human heart.Journal of Clinical Investigation, 1988
- Neurohormonal interactions and adaptations in congestive heart failure.Circulation, 1988
- Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure.Circulation, 1987
- Study of the normal and failing isolated human heart: Decreased response of failing heart to isoproterenolAmerican Heart Journal, 1983
- Decreased Catecholamine Sensitivity and β-Adrenergic-Receptor Density in Failing Human HeartsNew England Journal of Medicine, 1982
- Augmentation of the Plasma Nor-Epinephrine Response to Exercise in Patients with Congestive Heart FailureNew England Journal of Medicine, 1962