Dobutamine and the coronary vasomotion paradox.

Dobutamine, a structural relative of dopamine, acts directly on alphaand beta-adrenergic receptors without the release of norepinephrine or activation of dopaminergic receptors. For clinical use, dobutamine is a racemic mixture of a levo-isomer acting as a potent alpha-1 agonist and a dextro-isomer counterbalancing this effect as an alpha-1 antagonist. Both isomers are complete beta-receptor agonists with the dextro-isomer 10-fold more potent than the levo-isomer (1). Intravenous dobutamine is widely used to determine the significance of coronary atherosclerotic disease (2) and to support the myocardium during heart failure (3). Depending on dose, dobutamine has been demonstrated to evoke myocardial ischemia and identify myocardial hibernation and viability (4,5).