This study undertook a detailed examination of the ventricular-vascular interaction of the predominant -adrenergic agonist dobutamine using wave intensity analysis. Eight anesthetized open-chest ewes were instrumented with an aortic micromanometer to measure central aortic blood pressure (P) and an ultrasonic flow probe to obtain ascending aortic blood velocity (U). Hemodynamics were recorded during incremental dobutamine infusion (0.5, 1, 2.5, 5, 7.5 and 10 µg/kg/min). Wave intensity (dI_W) was calculated as the product of the rates of change of P and U with customized software using ensemble-averaged signals. Forward and backward components of dI_W, P and U were determined after calculation of wave speed. As well as the typical initial forward compression wave (FCW), mid-systolic backward compression wave (BCW) and late-systolic forward expansion wave (FEW_es), two minor and previously unheralded waves were also detectable in the wave intensity profile at baseline. The first was an early-systolic backward expansion wave (BEW), which reduced P but increased peak U. The second was a mid-systolic forward expansion wave (FEW_ms), which reduced P and U. During dobutamine infusion FCW dI_W increased 18-fold (P < 0.001), but BCW dI_W rose 12-fold (P < 0.001) while FEW_es dI_W fell by 70% (P < 0.001). However, the latter changes were accompanied by a 44-fold increase in BEW dI_W (P = 0.005) that augmented the initial aortic forward flow, and a >100 fold rise in FEW_ms dI_W (P < 0.001) that produced earlier and enhanced aortic blood deceleration. These findings provide new insights into the ventricular-vascular interaction of dobutamine.