Abstract

We investigated the hypothesis that the capacity of left ventricular myocardium to respond to an inotropic challenge by dopamine would be diminished in left ventricular hypertrophy induced by plication of the aortic valve. Seven mongrel dogs (LVH group) aged 6-8 weeks and weighing 4-6 kg, were subjected to preliminary surgery in which the noncoronary sinus of Valsalva was plicated. Six months later these animals, as well as a control group of dogs, were subjected to acute experiments in which the effect of dopamine (7.5 and 15 micrograms/kg/min) on regional and global myocardial function and oxygen consumption was studied. Myocardial segment length was measured with ultrasonic dimension transducers, and left ventricular and aortic blood pressures were recorded from catheter-tip transducers. Regional coronary blood flow was determined with radioactive microspheres, and regional oxygen saturation in small arteries and veins was measured using microspectrophotometry. Regional myocardial O2 consumption was calculated from these parameters. Heart weights were significantly elevated in the LVH group, and a pressure gradient of about 25 mm Hg was observed across the aortic valve. In both groups, dopamine infusion produced a dose-dependent increase in heart rate, left ventricular pressure, and LV dP/dtmax. Prior to dopamine infusion, percent shortening per beat was greater in the LVH group (13.97 +/- 1.2%) than in the control group (9.49 +/- 1.07%). Although the maximum speed of segment shortening was elevated by dopamine in both groups, percent shortening was not elevated in the LVH group. Stimulation by the high dose of dopamine produced a threefold elevation in regional coronary blood flow in both groups. Oxygen extraction was unchanged; the proportion of small veins with low O2 saturation was not elevated in LVH hearts, even during dopamine stimulation. Regional myocardial O2 consumption was elevated by dopamine (15 micrograms/kg/min) to about the same extent in both the control and LVH groups (19.1 +/- 2.3 and 17.5 +/- 2.3 ml O2/min/100 g) respectively. It is concluded that, in dogs with six months of aortic stenosis, dopamine does not exhaust functional reserve and the relationship between O2 supply and consumption is not significantly impaired.

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