Lipid and carbohydrate metabolism in the ischaemic heart.
Ischaemia has profound effects on myocardial metabolism and cell function in general. High energy phosphate and glycogen stores are depleted. Lactate, inorganic phosphate and hydrogen ions accumulate, exerting negative effects on the initially accelerated glycolytic flux. Fatty acid oxidation is inhibited. The cellular content of lipid intermediates, such as hydroxy-fatty acids, acyl CoA and acylcarnitine, increases in low-flow ischaemia hearts. Non-esterified fatty acid (NEFA) accumulation occurs after 30-60 min ischaemia. Endogenous triacylglycerol and phosphoglyceride turnover is most likely impaired, ultimately resulting in accumulation of lipid droplets in the oxygen deprived cells and in degradation of myocardial membranes. Accumulated lipid substances such as NEFA, acyl CoA, acylcarnitine and lysophosphoglycerides, are likely to be involved in the mechanism underlying ischaemia-induced damage to myocardial cells.
van der Vusse
G J
GJ
Dept. of Physiology, Medical Faculty Maastricht, University of Limburg, The Netherlands.
Stam
H
H
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D050260:Carbohydrate Metabolism; D003327:Coronary Disease / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005609:Free Radicals; D050356:Lipid Metabolism; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism
D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D005609:Free Radicals; D000255:Adenosine Triphosphate; D010100:Oxygen