Key result
Dopamine increased heart rate and contractility dose-dependently in dogs with experimental myocardial infarction, while peripheral and renal vascular resistance decreased at lower doses but increased at 20 μg/Kg/min.
Why the study?
Does intravenous dopamine alter hemodynamic parameters in a canine model of experimental myocardial infarction?
Does intravenous dopamine alter hemodynamic parameters in a canine model of experimental myocardial infarction?
In a canine model of myocardial infarction, dopamine demonstrated dose-dependent hemodynamic effects, suggesting potential utility in treating shock states.
Answers are grounded in this paper and cite their sources.
Dose-dependent hemodynamic effects support lower-dose dopamine in canine MI; extends preclinical data but leaves open human translation.
Hemodynamic effects of dopamine were studied on 30 open-chest dogs with experimental myocardial infarction. These dogs were divided into 3 groups. Three different doses of intravenous dopamine, 5, 10, and 20 mug/Kg/min, were administered for 30 min. Heart rate and myocardial contractility were increased dose-dependently. Total peripheral vascular resistance was reduced with 5 or 10 mug/Kg/min of dopamine. With 20 mug/Kg/min of dopamine, it became the lowest 5 min after the initiation of infusion but increased above the control value 20 min after the start of administration. Renal vascular resistance was decreased with 5 mug/Kg/min of dopamine but increased with 20 mug/Kg/min. These results suggested that this drug would be useful for treatment of shock state.
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Shozo Takeuchi (1975) studied Experimental myocardial infarction (n=30). Dopamine vs. Baseline (pre-infusion) was evaluated on Hemodynamic parameters (heart rate, myocardial contractility, vascular resistance). Dopamine increased heart rate and contractility dose-dependently in dogs with experimental myocardial infarction, while peripheral and renal vascular resistance decreased at lower doses but increased at 20 μg/Kg/min.
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