| Indication | For inotropic support in the short- term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures |
| Pharmacodynamics | Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the beta-adrenoceptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. Dobutamine acts primarily on beta-1 adrenergic receptors, with little effect on beta-2 or alpha receptors. It does not cause the release of endogenous norepinephrine, as does dopamine. Dobutamine is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures. |
| Mechanism of action | Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output. |
| Absorption | Not Available |
| Volume of distribution | Not Available |
| Protein binding | Not Available |
| Metabolism | Not Available |
| Route of elimination | In human urine, the major excretion products are the conjugates of dobutamine and 3-O-methyl dobutamine. |
| Half life | 2 minutes |
| Clearance | Not Available |
| Toxicity | Not Available |