Effect of dopamine and calcium on lipolysis and myocardial ischemic injury following acute coronary occlusion in the dog.

Ischemic myocardial injury was quantified as the sum of S-T segment elevations in epicardial electrocardiogram recordings (2S-T) following acute coronary artery occlusions in 17 dogs. 2S-T rose from 3 ± 1 mv to 26 ± 4 mv (P < 0.001) following occlusion. Myocardial contractility was similarly stimulated by intravenous infusions of dopamine or calcium. At reocclusions of the coronary artery, 2S-T increased to 73 ± 12 mv (P < 0.001) with dopamine and to 41 ± 7 mv (P < 0.001) with calcium; the difference was statistically significant (P < 0.005). Arterial concentrations of free fattv acids (FFAa) were raised from 248 ± 33 /iEq/liter to 888 ±161 /u.Eq/liter (P < 0.005) with dopamine, but administration of calcium did not influence FFAa. After inhibition of lipolysis with /3-pyridyl carbinol, no difference in 2S-T or FFAa was observed; the mean values were 31 ± 4 mv for 2S-T and 144 ± 13 /iEq/liter for FFAa. Myocardial lipolysis was suggested in three experiments in which /3-pyridyl carbinol reduced XS-T with dopamine, although FFAa remained unchanged. These measurements suggest that dopamine-induced lipolysis contributes significantly to the enlargement of ischemic injury in the myocardium following acute coronary artery occlusion, probably due to the metabolic stimulation of myocardial oxygen requirements. Test doses of dopamine given to seven patients raised FFAa by 225 ± 87 /xEq/liter (P < 0.03).