Does experimental heart failure alter the uptake and retention of norepinephrine in the heart?
Experimental heart failure in guinea pigs leads to depletion of cardiac norepinephrine stores due to a defect in its uptake and/or retention.
The present study was undertaken to evaluate the influence of heart failure on the cardiac stores of norepinephrine, and to elucidate the mechanisms responsible for the changes observed. Congestive heart failure was produced in the guinea pig by supravalvular aortic constriction. Significant reductions in both the concentration and content of norepinephrine in the ventricles were observed, the magnitude of changes being related to the severity of the constriction. The renal concentration of norepinephrine was not usually affected. Infusions of large quantities of norepinephrine produced elevations of ventricular norepinephrine concentrations which were significantly less in guinea pigs with heart failure than in normal animals. Injections of lesser quantities of radioactive norepinephrine also resulted in smaller amounts of this material in the hearts of animals with failure. Measurement of the decay of specific activity indicated that heart failure did not alter the net turnover of norepinephrine in the left ventricle. From these findings it has been concluded that a defect in the uptake and/or retention of norepinephrine exists in these hearts and that this defect may be responsible for the depletion of norepinephrine.
Spann et al. (1965) studied this question.