Effects of dobutamine on left ventriculoarterial coupling and mechanical efficiency in acutely ischemic pigs

This study investigated the effects of dobutamine on left ventriculoarterial (VA) coupling and mechanical efficiency in acutely ischemic pigs. Experiments were performed in 12 pigs in which vascular properties, including peripheral resistance (R-2), compliance (C), and arterial elastance (E-a), were estimated with a windkessel model, and left ventricular (LV) function by the slope (E-es) of the end-systolic pressure-volume relationship (ESPVR) and stroke work (SW). VA coupling was defined as E-es/E-a, and mechanical efficiency as SW/pressure-volume area (PVA). In all animals, the left anterior descending coronary artery was ligated after basal measures. The animals were then randomly divided into 2 groups: group CTRL (n = 6) was followed for 180 minutes without other intervention, whereas group DOBU (n = 6) was infused with dobutamine (5 mug(.)kg(-1.)min(-1)) starting after T60 measures. Coronary occlusion induced a rightward shift of ESPVR and a decrease in E-es from 3.67 +/- 0.33 to 1.92 +/- 0.20 mm Hg(.)mL(-1), while E-a changed from 3.33 +/- 0.56 to 4.65 +/- 0.29 mm Hg(.)mL(-1), R-2 from 1.72 +/- 0.30 to 2.38 +/- 0.16 mm Hg(.)s(.)mL(-1), and C from 0.78 +/- 0.16 to 0.46 +/- 0.08 mL(.)mm Hg-1. This altered VA coupling from 1.22 +/- 0.11 to 0.44 +/- 0.07. SW decreased from 4056 +/- 223 to 2372 +/- 122 mm Hg(.)mL, and PVA and SW/PVA decreased from 5575 +/- 514 to 4830 +/- 3.17 mm Hg(.)mL, and from 0.76 +/- 0.04 to 0.49 +/- 0.03, respectively. In group DOBU, dobutamine restored E-es and the position of ESPVR to baseline values, while E-a decreased to 3.39 +/- 0.34 mm Hg(.)mL(-1) because of an R-2 decrease to 1.60 +/- 0.24 mm Hg(.)s(.)mL(-1). VA coupling was restored. SW and PVA increased to 3833 +/- 180 mm Hg(.)mL and to 7498 +/- 442 mm Hg(.)mL, respectively, while SW/PVA was unchanged. In ischemic pigs, dobutamine restored VA coupling through an increase in LV contractility and decrease in arterial elastance as a result of peripheral vasodilatation. However, myocardial oxygen consumption was increased, and mechanical efficiency impaired.