Dobutamine, a synthetic catecholamine, increases cardiac output and corrects hypoperfusion. It acts on α1-AR, β1-AR, and β2-AR (α-1, β-1, and β-2 adrenoceptors) with selective agonist activity on β1-AR and relatively weak activity at α1-AR and β2-AR. [1] [2] [3] [4].

Dobutamine rapidly initiates action and possesses a short half-life. Administered intraperitoneally at dosages ranging from 0.15 to 20 mg/kg, it enhances left ventricular function and escalates heart rate in wildtype mice, with effects intensifying at higher doses. At elevated doses, dobutamine significantly amplifies inotropic (force of heart's contraction), lusitropic (relaxation of cardiac muscles), and chronotropic (rate of heartbeat) responses in these mice. Conversely, low doses markedly improve inotropic and lusitropic functions without affecting heart rate in Tgαq*44 mice, models of heart failure, indicating a dose-dependent variability in cardiac response. However, beyond certain dosages, dobutamine increases heart rate without improving cardiac functional reserve, underlining a lost benefit in heart function at high doses. Additionally, dobutamine has been shown to increase alveolar liquid clearance in ventilated rats through beta-2 receptor stimulation, showcasing its potential benefits beyond cardiac applications.