Why the study?
Does inhibition of lipolysis reduce myocardial oxygen consumption during isoproterenol infusion in intact and anesthetized dogs?
Does inhibition of lipolysis reduce myocardial oxygen consumption during isoproterenol infusion in intact and anesthetized dogs?
Inhibition of lipolysis reduces the isoproterenol-induced increase in myocardial oxygen consumption in dogs, suggesting that high free fatty acid concentrations metabolically stimulate oxygen demand.
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Attenuates catecholamine-driven myocardial oxygen demand in dogs; leaves open translation to human metabolic therapies.
The effect of intravenous infusion of isoproterenol on myocardial oxygen consumption (MVo(2)) was studied in 10 intact and anesthetized dogs before and after inhibition of lipolysis. In five dogs lipolysis was inhibited by nicotinic acid or beta pyridyl carbinol and in five other dogs by high plasma glucose concentrations. In spite of similar mechanical responses to isoproterenol, as evidenced by left ventricular pressure, maximal rate of rise of left ventricular pressure (dP/dt), heart rate and cardiac output, augmentation of MVo(2) was larger before (on average 7.6 ml/min.100 g) than after inhibition of lipolysis either by antilipolytic drugs (on average 4.5 ml/min.100 g) (P < 0.005), or by high plasma glucose concentrations (on average 4.3 ml/min.100 g) (P < 0.02). As mechanical responses to isoproterenol were similar before and after inhibition of lipolysis, it is concluded that the additional rise in MVo(2) with intact lipolysis was caused by a metabolic stimulation by high concentrations of free fatty acids.
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Ole D. Μjøs (1971) studied this question.
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