Lipid and Carbohydrate Metabolism of Myocardium During the Biphasic Inotropic Response to Epinephrine

The metabolic response of the left ventricle to a 90 min regional infusion of 1-epinephrine (5 µg/min) was assessed in the intact anesthetized dog for 3 hr. The first hour was characterized by a rise in stroke output at constant filling pressure. Subsequently, contractility fell and there was release of K and PO 4 ions as well as SGOT from the myocardium that was attributed to tissue injury. The myocardial RQ rose for the first hour, presumably due to glycogenolysis, since carbohydrate extraction from blood was unaltered. Production of lactate by the myocardium during the RQ rise occurred without ischemia, since blood flow (Kr 85 method) and O 2 uptake rose 10%. The proportionately greater increase in contractility was not consistent with "O 2 wasting" as a basis for the injury. After 1 hr the RQ fell to levels consistent with predominant lipid utilization. However, FFA extraction declined and the oxidation, extraction and incorporation of palmitate-l-C 14 into tissue lipid were diminished during hormone exhibition. Plasma triglyceride uptake, insignificant in controls, was enhanced during the 3 hr without a rise in arterial concentration. Oxidation of this lipid was insufficient to prevent a threefold triglyceride increment in the myocardium. The authors discuss a possible relationship of these metabolic alterations to the pathophysiologic response induced by epinephrine.