Why the study?
Does Aramine improve cardiovascular hemodynamics in an experimental model of ventricular failure?
Does Aramine improve cardiovascular hemodynamics in an experimental model of ventricular failure?
Aramine improves myocardial contractility and reverses experimental ventricular failure, challenging the premise that cardiogenic shock agents should act solely on the peripheral vascular bed.
Challenges vascular-only paradigm for shock agents; hypothesis-generating for inotropes in failure, pending clinical translation.
The cardiovascular effects of a new, long-acting, sympathomimetic amine, Aramine, are described. Cardiac output, aortic pressure, coronary flow, and ventricular stroke work rise while atrial pressures fall. A sustained increase in myocardial contractility is produced and the myocardium does not require more coronary flow per unit of ventricular work after its administration. The circulatory effects of ventricular failure produced by restricting coronary flow are reversed by the drug. The authors seriously question the premise that the ideal agent for the management of cardiogenic shock should act solely on the peripheral vascular bed.
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Sarnoff et al. (1954) studied this question.
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