Key result
Cocaine infusion markedly prolongs the decay of chronotropic and inotropic responses in dogs.
Why the study?
The relative efficacy of neuronal uptake in dissipating neurally released norepinephrine among different cardiac tissues was unclear.
Neuronal uptake of norepinephrine is most effective in the sinoatrial node, less in the atrial myocardium, and least in the ventricular myocardium.
Highlights regional norepinephrine uptake gradients; hypothesis-generating for cocaine effects pending human data.
The cardiac responses to sympathetic nerve stimulation were measured in open-chest, anesthetized dogs before and after infusions of cocaine, which were given to inhibit the neuronal uptake of norepinephrine. Cocaine did not augment the inotropic or chronotropic responses, but it did retard their decay after cessation of sympathetic stimulation. Before cocaine, the half-times for decay of the chronotropic, atrial inotropic, and ventricular inotropic responses were 28.4 +/- 2.2, 29.8 +/- 2.7, and 22.1 +/- 1.9 (+/- SE) s, respectively. After cocaine, however, the half-times were significantly greater (147 +/- 12.0, 51.4 +/- 3.9, and 32.9 +/- 2.5 s, respectively). The cocaine-induced prolongation of the decay time in a given cardiac tissue is a measure of the relative efficacy of neuronal uptake as a mechanism for dissipating the neurally released norepinephrine. Our data indicate, therefore, that among the various cardiac tissues that we studied, the neuronal uptake mechanism is least effective in the ventricular myocardium, somewhat more effective in the atrial myocardium, and most effective in the sinoatrial nodal region.
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Masuda et al. (1985) studied this question. Cocaine infusion vs. Before cocaine infusion was evaluated on Half-times for decay of chronotropic, atrial inotropic, and ventricular inotropic responses. Cocaine infusion significantly prolonged the decay half-times of chronotropic (147 vs 28.4 s), atrial inotropic (51.4 vs 29.8 s), and ventricular inotropic (32.9 vs 22.1 s) responses in dogs.
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