Circulation, Vol 65, 1321-1328, Copyright © 1982 by American Heart Association
RE Rude, C Izquierdo, LM Buja and JT Willerson
The effect of i.v. dobutamine on acute myocardial ischemic injury was
assessed in 22 anesthetized dogs subjected to serial 10-minute occlusions
of the left anterior descending coronary artery. The severity of ischemic
injury was determined by mass spectrometric measurement of the increase in
intramural carbon dioxide tension (delta PmCO2) in the ischemic zone. In
the time protocol 1 dogs, dobutamine, 20 micrograms/kg/min, infused between
the control and final occlusion, significantly increased both heart rate
(HR) and left ventricular (LV) dP/dt; delta PmCO2 was significantly higher
during the dobutamine infusion that during control occlusion (76 +/- 21 vs
56 +/- 13 mm Hg, p less than 0.01). The nine protocol 2 dogs were atrially
paced at a HR of 20--30 beats/min above baseline values during the control
occlusion and received dobutamine (12.6 +/- 7.8 micrograms/kg/min) at doses
necessary to attain an equal HR (mean 149--154 beats/min) during the last
occlusion. Although LV dP/dt was higher after dobutamine, delta PmCO2 was
similar during the two occlusions. Protocol 3 dogs (n = 4) received lower
doses of dobutamine (5.6 +/- 3.2 micrograms/kg/min) to produce an increase
in LV dP/dt, but not in HR compared with baseline values; delta PmCO2 was
similar during control and dobutamine occlusions. There were no major
change in arterial or left atrial pressures. Rate-pressure product, an
indirect measurement of myocardial oxygen consumption, was increased only
by the higher doses of dobutamine in protocol 1. Thus, inotropic
stimulation with dobutamine during coronary occlusion does not cause
important augmentation of acute myocardial ischemic injury in the
nonfailing heart unless HR is increased simultaneously.
ARTICLES
Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. I. Studies with dobutamine in the anesthetized dog
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