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Research Article Free access | 10.1172/JCI106167

Autonomic blockade by propranolol and atropine to study intrinsic myocardial function in man

Anthony D. Jose and Roger R. Taylor

Hallstrom Institute of Cardiology, Sydney, Australia

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

Hallstrom Institute of Cardiology, Sydney, Australia

Find articles by Taylor, R. in: JCI | PubMed | Google Scholar

Published November 1, 1969 - More info

Published in Volume 48, Issue 11 on November 1, 1969
J Clin Invest. 1969;48(11):2019–2031. https://doi.org/10.1172/JCI106167.
© 1969 The American Society for Clinical Investigation
Published November 1, 1969 - Version history
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Abstract

Blockade of cardiac autonomic nervous activity by an intravenous injection of 0.2 mg/kg propranolol and 0.04 mg/kg atropine was used with cardiac catheterization to study intrinsic cardiac function in 47 patients with normal hearts and known graded myocardial disease. After blockade, significant hemodynamic abnormalities became apparent at rest in the majority of patients with known disease, many of whom had normal control findings. This occurred partly through a reduction in the normal range of cardiac function at rest, and partly through changes in the abnormalities associated with disease: after blockade, diseased hearts had normal stroke volumes, but beat more slowly, and had higher left ventricular filling pressures. The heart rate after blockade was fixed; this was defined as the intrinsic heart rate (IHR); it ranged from 57 to 126 beats/min in different patients. Both the IHR and left ventricular end-diastolic pressure after blockade were sensitively and quantitatively related to the severity of myocardial disease. When, after blockade, arterial pressure was raised by angiotensin, the IHR was unchanged; normal hearts maintained their stroke volume and increased stroke work; diseased hearts maintained stroke volume less well and stroke work was unchanged or fell. Abnormal ventricular responses corresponded well with abnormal ventricular function at rest.

In different patients the IHR was significantly related to each available index of left ventricular function. Other studies in animals have shown that the IHR is closely related to intrinsic myocardial contractility in certain forms of experimental heart failure. An analogous relationship existing between the IHR and myocardial function in patients with heart disease is suggested as the explanation for the IHR/ventricular function relationship in this study. If so, the IHR may prove valuable as an index of myocardial function in man, since it can be measured simply and safely in clinical practice.

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