Influence of free fatty acids on myocardial oxygen consumption and ischemic injury.
Myocardial oxygen consumption (MVO2) is influenced by the substrate supply to the heart. Utilization of free fatty acids increases MVO2, and catecholamines sensitize the heart to the oxygen-wasting effect of free fatty acids. Alteration of myocardial metabolism from mainly free fatty acid to carbohydrate oxidation reduces the extent of myocardial ischemic injury. Within the ischemic myocardium, lipolysis is stimulated with breakdown of endogenous triglycerides to fatty free acids and glycerol. Antilipolytic agents seem to have a combined effect on myocardial metabolism partly through inhibition of lipolysis in adipose tissue with reduction of free fatty acid mobilization to plasma, and partly through a local inhibition of lipolysis in the ischemic myocardium. In patients with high sympathoadrenal activity, for example, patients with acute myocardial ischemia in unstable ischemic heart disease, elevation of free fatty acids might effect a critical increase in both myocardial oxygen requirement and infarct size.
D000273:Adipose Tissue / Q000378:metabolism; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D050260:Carbohydrate Metabolism; D002395:Catecholamines / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D008066:Lipolysis / Q000187:drug effects; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009539:Nicotinic Acids / Q000494:pharmacology; D010101:Oxygen Consumption; D014280:Triglycerides / Q000378:metabolism
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D009539:Nicotinic Acids; D014280:Triglycerides; D005990:Glycerol