Why the study?
Does dopamine increase ischemic myocardial injury compared to calcium following acute coronary occlusion in dogs?
Does dopamine increase ischemic myocardial injury compared to calcium following acute coronary occlusion in dogs?
Dopamine-induced lipolysis appears to exacerbate ischemic myocardial injury during acute coronary occlusion, suggesting a metabolic mechanism for increased oxygen demand.
Dopamine may worsen ischemic injury via lipolysis in canine models; leaves open translation to human acute coronary syndromes.
Ischemic myocardial injury was quantified as the sum of S-T segment elevations in epicardial electrocardiogram recordings (ΣS-T) following acute coronary artery occlusions in 17 dogs. ΣS-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, ΣS-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 (FFA a ) were raised from 248 ± 33 µEq/liter to 888 ± 161 µEq/liter ( P < 0.005) with dopamine, but administration of calcium did not influence FFA a . After inhibition of lipolysis with β-pyridyl carbinol, no difference in ΣS-T or FFA a was observed; the mean values were 31 ± 4 mv for ΣS-T and 144 ± 13 µEq/liter for FFA a . Myocardial lipolysis was suggested in three experiments in which β-pyridyl carbinol reduced ΣS-T with dopamine, although FFA a 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 FFA a by 225 ± 87 µEq/liter ( P < 0.03).
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Lekven et al. (1974) studied this question.
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