Cardiac Norepinephrine Stores in Experimental Heart Failure in the Dog*

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Abstract
The recent observation that myocardial norepinephrine concentration is reduced in patients withcongestive heart failure suggested that a depletion of neurotransmitter store may occur in this condition. This possibility was examined in experimental congestive heart failure, which was produced in 8 dogs by creation of tricuspid insufficiency and pulmonic stenosis. When killed 6 to 8 weeks later, ascites and hepatic congestion were present in all animals. The concentration and total amount of norepinephrine in both ventricles was strikingly reduced, the latter averaging 0.15 and 0.63 [mu]g per kg body weight, respectively, in right and left ventricles, compared to 1.14 and 3.89 [mu]g per kg in control dogs. In spite of this depletion of ventricular norepinephrine, uptake and binding of a tracer dose of radioactive norepinephrine was not significantly reduced in the animals with heart failure. The effects of tyramine were studied in isolated right ventricular papillary muscle preparations. The maximal increase in contractile force produced by tyramine averaged 138% above control in muscles from normal dogs and less than 20% in muscles from dogs with heart failure. It is concluded that depletion of norepinephrine stores occurs in congestive heart failure, and it is suggested that this depletion may interfere with transmission of sympathetic nerve impulses to the heart and thereby adversely affect myocardial performance.