Abstract
The effects of epinephrine on contractility and metabolism were measured in the isolated, perfused rat heart. Epinephrine produced an initial increase in force of contraction followed by a lowering of tension and finally a sustained increase in contractility. When fluoroacetate or iodoacetate was present in the perfusion fluid, the mechanical response to epinephrine was markedly altered. The initial response to epinephrine was depressed in the presence of either inhibitor and the final increase in force of contraction was poorly maintained during metabolic blockade. When the perfusion fluid contained both pyruvate and iodoacetate, the mechanical response of the heart to epinephrine was restored. Results of determinations of metabolites in the myocardium demonstrated that stimulation of glycogenolysis is not essential for the contractile response to epinephrine when adequate substrate is provided for the reactions of the tricarboxylic acid cycle.
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