Key result
Nicotinic acid reverses catecholamine-induced increases in myocardial oxygen consumption.
Why the study?
The study aimed to understand the factors determining myocardial oxygen consumption during elevation of aortic blood pressure, focusing on metabolic influences beyond mechanical activity.
FFA may drive excess myocardial O2 demand independently of workload; leaves open translation to human ischemia therapy.
Myocardial oxygen consumption (MO2) is substantially raised in dogs by isoproterenol infusion, but subsequent infusion of angiotensin causes only a small additional increase. These effects on MO2 are reversed after inhibition of lipolysis with nicotinic acid, indicating that a metabolic factor related to high plasma concentrations of free fatty acids (FFA) increases MO2, regardless of the changes in mechanical activity.
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Mjøs et al. (1972) studied this question. Isoproterenol, angiotensin, and nicotinic acid infusions was evaluated on Myocardial oxygen consumption (MO2). Inhibition of lipolysis with nicotinic acid reversed increases in myocardial oxygen consumption caused by isoproterenol and angiotensin in dogs.
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