To determine whether changes in left ventricular catecholamine content occur during the first 30 to 90 min of acute myocardial infarction, myocardial catecholamine (radioenzymatic assay) over the interval was studied in the dog. In nine pentobarbital-anesthetized opened-chest dogs without coronary ligation, myocardial catecholamine at 2.5 h after pentobarbital (i) consisted mainly of norephinephrine (87% total catecholamine), (ii) showed a base to apex gradient in norephinephrine (1.44 ± 0.10 vs. 1.03 ± 0.10 μg/g, p < 0.05) and dopamine (0.20 ± 0.03 vs. 0.12 ± 0.02 μg/g, p < 0.05) but not epinephrine (0.017 vs. 0.016 μg/g), and (iii) showed no difference in norepinephrine, dopamine, or epinephrine across basal, mid, and apical left ventricular transverse planes spanning the vascular territories of the two coronary arteries. In 18 pentobarbital-anesthetized dogs with coronary ligation, (i) norepinephrine, measured in 14 regions across the mid left ventricle after 90 min ischemia in four dogs, was less in the ischemic center of the occluded bed than normal myocardium (1.01 ± 0.04 vs. 1.29 ± 0.04 μg/g, p < 0.05), and (ii) norepinephrine was unchanged in normal myocardium of 14 dogs at 30, 60, 90 min, and 48 h but decreased in ischemic myocardium by 31% at 60 min (0.89 ± 0.10 vs. 1.29 ± 0.08 μg/g, p < 0.025) and 79% at 48 h (0.27 ± 0.04 vs. 1.26 ± 0.08 μg/g, p < 0.001). Thus, norepinephrine depletion from ischemic but not normal myocardium is detectable by 60 min during acute myocardial infarction.
BLOOD SEROTONIN LEVELS IN DOGS WITH ACUTE MYOCARDIAL INFARCTION PRODUCED BY CORONARY LIGATION
