Why the study?
Does intravenous sodium salicylate alter myocardial free fatty acid uptake and oxygen consumption in anesthetized dogs?
Does intravenous sodium salicylate alter myocardial free fatty acid uptake and oxygen consumption in anesthetized dogs?
Sodium salicylate reduces myocardial oxygen consumption during isoproterenol infusion, likely mediated by reduced myocardial free fatty acid consumption.
Attenuates isoproterenol-driven MVO2 in dogs; leaves open whether salicylate alters human myocardial metabolism or outcomes.
The effect of sodium salicylate on net myocardial free fatty acid (FFA) uptake, myocardial oxygen consumption (MVO2), and the mechanical activity of the heart was studied in eight intact, anesthetized dogs. Sodium salicylate was given intravenously under basal conditions and during isoproterenol-stimulated lipolysis. Under basal conditions, sodium salicylate significantly reduced arterial FFA concentration, but did not influence net myocardial uptake of FFA, and MVO2 was unchanged. During isoproterenol infusion sodium salicylate reduced arterial FFA concentration 28% (P less than 0.01) and significantly reduced net myocardial uptake of FFA from 44.5 +/- 9.0 (mean +/- S.E.M.) to 22.3 +/- 2.1 mumol/min-100g tissue (P less than 0.05) and MVO2 from 20.3 +/- 2.2 to 160 +/- 1.9 ml/min-100g tissue (P less than 0.05). The reduction in MVO2 could not be explained by reduced mechanical activity of the heart. Most probably the mechanism for the reduction in MVO2 effected by sodium salicylate during isoproterenol infusion was mediated by reduced myocardial FFA consumption.
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Vik‐Mo et al. (1976) studied this question.
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