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Canadian Journal of Anesthesia, Vol 16, 336-344, Copyright © 1969 by Canadian Anesthesiologists' Society
1 Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York
The effect of beta-adrenergic blockade produced by propranolol (0.25 mg/kg) on myocardial haemodynamics and metabolism was investigated in eight closed-chest dogs lightly anaesthetized with halothane (0.69% expired). A significant decrease in cardiac output and left ventricular stroke work was seen, with increases in left ventricular end diastolic pressures, mean aortic pressure, and peripheral vascular resistance. There was no change in heart rate, right atrial pressure, or the rate of rise of left ventricular pressure (dp/dt). Myocardial blood flow, oxygen uptake, and excess lactate were likewise unchanged. There was no significant difference between the control and beta-blocked animals in the arterial levels or in regard to the myocardial uptake of glucose, non-esterified fatty acids, lactate, or pyruvate. It appeared that the myocardial depression produced by beta adrenergic blockade in these animals was offset by the increased peripheral vascular resistance and mean aortic blood pressure. It is suggested that were such compensation not possible, the effect of beta-adrenergic blockade in light halothane anaesthesia might be more deleterious.
Note:
Supported in part by a grant from the Genesee Valley Heart Association. Mr. Tonnesen's work was carried out during a medical student summer fellowship with support of US Public Health Service grsg grant fro 5403.
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