Lysophosphoglycerides, products of membrane phospholipid catabolism known to influence membrane function in several systems, appeared in the effluents of anoxic isolated rabbit hearts perfused at low flow and accumulated in perfused hearts and myocardium rendered ischemic in situ. Comparable concentrations of lysophosphoglycerides bound to albumin markedly and reversibly altered action potentials of isolated canine Purkinje fibers in vitro. Changes induced included diminution of the maximum diastolic potential, peak dV/dt of phase zero, amplitude, and action potential duration--alterations resembling those seen in ischemic myocardium in vivo. These electrophysiological alterations are compatible with changes implicated in predisposing to dysrhythmia dependent on reentry, a phenomenon potentiated by the presence of zones of decreased conduction. Thus, accumulation of lysophosphoglycerides induced by ischemia may contribute to the genesis of malignant dysrhythmia early after its onset.

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Accumulation of lysophosphoglycerides with arrhythmogenic properties in ischemic myocardium.

Modifications in dietary fat profile have been shown to affect body weight gain and adiposity. This may occur through changes in the partitioning between oxidation and storage and/or alterations in membrane structure, which may in turn influence metabolic rate. All the dietary fat classes are substrates for the biosynthetic elongase and desaturase enzymes. Obesity is associated with increased delta 9 desaturase activity, reduced delta 5 desaturase activity and perhaps reduced delta 6 desaturase activity. Dietary lipid profile can affect the activity of each of these enzymes. A number of possible mechanisms linking dietary fat subtypes with development of obesity are discussed, including modification of sodium potassium pump activity and alterations in mitochondrial proton leakage.

Dietary fats, membrane phospholipids and obesity.

The effects of 5, 10 and 20% dietary menhaden oil (MO) on the composition of heart lipid classes and fatty acids were studied. Male Sprague-Dawley rats were fed ad libitum 0, 5, 10 and 20% MO for 3 wk. The heart phosphoglyceride content and composition and cholesterol were unchanged by dietary MO. A nonlinear dose-response relationship was observed between dietary MO levels and fatty acid compositional changes. Cardiolipin, choline (PC), ethanolamine (PE) and serine/inositol (PS/PI) phosphoglycerides showed an incorporation of n-3 fatty acids, eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3), between the control and 5% MO group, a plateau between the 5 and 10% MO groups and a further increase at the 20% MO level. The initial reduction in 20:4n-6 content remained unchanged as dietary MO increased except in PE where a further reduction was found at the 20% MO level. Dietary MO did not significantly change the 20:4n-6 content in neutral lipids. Linoleic acid content was most resistant to dietary MO removal. The level of 18:2n-6 was significantly lowered in heart PC when rats were fed 10% MO. No significant differences were found in PS/PI. In PE and NL significant differences occurred only when rats were fed 20% MO. The significant fatty acid modifications of heart lipid and PL found between the control and lowest level of dietary MO (5%) suggest that dietary fish oil supplementation in human diets may not be required for this effect.

Dietary n-3 polyunsaturated fatty acids: modification of rat cardiac lipids and fatty acid composition.

1. The fatty acid composition of cardiac membrane lipids is influenced by age, sex, diet and other factors. 2. The relative amounts of various polyunsaturated fatty acids in cardiac lipids influence markedly the development of myocardial necrosis and mortality following overstimulation with isoproterenol. 3. The availability and metabolism of arachidonic acid may play an important role in regulation of cardiac metabolism.

The role of myocardial membrane lipids in the development of cardiac necrosis.

Lipids and cardiac arrhythmia.

Administration of isoproterenol induces changes in phospholipids of heart muscle membranes. Longer and more unsaturated fatty acids replace shorter and less unsaturated fatty acids. Dietary polyunsaturated fatty acids, i.e., C22:6, replace C18:2 and C20:4 in phospholipids of heart muscle. Increased sensitivity to isoproterenol and increased myocardial cell damage is accompanied by a relative increase in long chain polyunsaturated fatty acids in phospholipids of heart muscle. Development of myocardial necrosis increases with a progressive replacement of C18:2 and C20:4 by C22:6. Alterations in fatty acid composition of membrane phospholipids and consequent changes in membrane properties may play an important role in myocardial cell damage. Myocardial damage following administration of isoproterenol is increased when there is enhanced intramyocardial lipolysis and an increased amount of polyunsaturated fatty acids in membrane phospholipids. Mocardial damage is decreased when there is reduced intramyocardial lipolysis and the membrane response makes the membranes less permeable and more stable.

Changes in fatty acid composition of cardiac lipids accompanying myocardial necrosis.

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Changes in fatty acid composition of cardiac lipids accompanying myocardial necrosis.