Dobutamine improves afterload-induced deterioration of mechanical efficiency toward maximal.
We studied the effect of increased afterload on the ratios of O2 consumption (VO2) to external work (EW), VO2 to the systolic pressure-volume area (PVA), and PVA to EW at control state and with dobutamine in the left ventricles of open-chest dogs. Left ventricular volume was measured with a volumetric conductance catheter and coronary flow with an electromagnetic flowmeter. Hexamethonium bromide and atropine sulfate were administered before changes in end-systolic pressure (Pes) with an infusion of nitroprusside or angiotensin II. Dobutamine enhanced ventricular end-systolic elastance by 100%. In the control, with increases in Pes, EW/VO2 remained unchanged, PVA/VO2 increased by 48%, and EW/PVA decreased by 26%. Dobutamine increased both EW/VO2 and EW/PVA at any given Pes but decreased PVA/VO2. During dobutamine, EW/VO2 increased significantly with increases in Pes. The ratio of measured EW/VO2 to the theoretically predicted maximal EW/VO2 value for a given end-diastolic volume and contractility was 0.83 at a Pes of 70 mmHg, and this ratio decreased by 33% with increases in Pes in the control. During dobutamine, measured EW/VO2 values were almost equal to each corresponding theoretical maximal value, and the average decrease in the ratio with increases in Pes was 7%. Thus the enhanced inotropic state by dobutamine can restore the afterload-induced deterioration of EW/VO2 toward the normal maximal level.
Nozawa
T
T
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Wada
O
O
Ishizaka
S
S
Asanoi
H
H
Fujita
M
M
Sasayama
S
S
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D004280:Dobutamine / Q000494:pharmacology*; D004285:Dogs; D006321:Heart / Q000187:drug effects*; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000187:drug effects*; D010101:Oxygen Consumption
D004280:Dobutamine