[Dobutamine: mechanisms of action and use in acute cardiovascular pathology].

High levels of circulating catecholamines associated with heart failure down-regulate cardiac beta-receptors, with a more pronounced effect on beta-1 receptors, leading to impaired inotropic effect. The use of exogenous inotropic agents is therefore a logical therapeutic approach in heart failure. Dobutamine is a synthetic catecholamine that acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a relatively weak chronotropic effect. In the vasculature, alpha-1 agonist activity (vasoconstriction) balances the beta-2 agonist effect (vasodilatation). In clinical use, dobutamine has a rapid onset of action and a short half-life. It increases myocardial contractility, while the reflex reduction in sympathetic tone, in response to augmentation of stroke volume, leads to a decrease in total peripheral resistance. The expected hemodynamic effects are an increase in cardiac output and a decrease in systemic vascular resistance without significant change in arterial pressure or heart rate. In acute cardiac failure state with elevated afterload pressures, resulting from myocardial dysfunction, dobutamine therapy remains, nowadays, the reference.