AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 263: H1201-H1207, 1992;
0363-6135/92 $5.00
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AJP - Heart and Circulatory Physiology, Vol 263, Issue 4 1201-H1207, Copyright © 1992 by American Physiological Society

ARTICLES

Dobutamine improves afterload-induced deterioration of mechanical efficiency toward maximal

T. Nozawa, O. Wada, S. Ishizaka, H. Asanoi, M. Fujita and S. Sasayama
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.

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.


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H. Asanoi, T. Kameyama, S. Ishizaka, T. Nozawa, and H. Inoue
Energetically Optimal Left Ventricular Pressure for the Failing Human Heart
Circulation, January 1, 1996; 93(1): 67 - 73.
[Abstract] [Full Text]


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