Abstract
The effects of two antibiotics, X-537A and A23817, which transport Ca 2+ as a lipid-soluble complex through a number of natural and artificial membranes, have been investigated using a perfused working rat heart preparation. When the contractility of the hearts was depressed by either low Ca 2+ concentration or by addition of ruthenium red to the perfusion medium, X-537A produced a large increase of coronary flow rate, left ventricular pressure development and work output. These effects were suppressed in the presence of propranolol and in the hearts from animals pretreated with reserpine. The other ionophore, A23187, was without significant effect on cardiac contractility but increased the coronary flow rate. These results suggest that the mechanism of action of X-537A in the isolated heart is not via an increased permeability of the plasma membrane to Ca 2+. The positive inotropic effect of X-537A is better explained as resulting from the release of endogenous norepinephrine.
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