Myocardial Extraction and Production of Catechol Amines

Stimulation of the cardiac sympathetic efferent nerves is accompanied by a release of catechol amines in coronary blood. This release is a function of stimulation intensity and occurs even when stroke volume and coronary outflow are maintained constant. Comparison between the ethylenediamine and the trihydroxyindole methods for the analysis of plasma catechol amines shows both quantitative and qualitative differences, with only the results with the latter method showing a consistent relationship to the hemodynamic changes observed during cardiac sympathetic stimulation. The acutely synipatheetomized heart extracts catechol amines from coronary blood in the absence of nervous stimulation. The patterns of extraction observed indicate that the quantity of catechol amines in the myocardium can modify the extent of extraction in the unstimulated state as well as the extent of release during stimulation. Continued stimulation of the cardiac sympathetics is accompanied by at least a partial depletion of the myoeardial catechol amine stores. These stores appear to be repleted by circulating catechol amines, since the response to any given intensity of stimulation can be potentiated by a prior norepinephrine infusion. Dichloroisoproterenol prevents neither the myocardial extraction of catechol amines in the unstimulated state nor the release of catechol amines during sympathetic stimulation; it does lessen or abolish the cardiody-namic effects of sympathetic stimulation. Data are presented which indicate that a direct coronary vasoconstriction is one of the consequences of cardiac sympathetic nerve stimulation, the vasodilatation usually observed being due, at least in part, to overriding metabolic factors.