This study undertook a detailed examination of the ventricular-vascular interaction of the predominant beta-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 microg.kg(-1).min(-1)). 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), midsystolic 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.