ABSTRACT
The effects of stearic, oleic, and arachidonic acids on phosphatidylcholine biosynthesis in the hamster heart were investigated. When hamster hearts were perfused with labelled choline in the presence of fatty acids, biosynthesis of phosphatidylcholine was stimulated only by stearic acid. Stearic acid was found to accumulate in unesterified (free) form in the hamster heart after perfusion. The stimulation by stearic acid was mediated in vivo by an enhancement of CTP:phosphocholine cytidylyltransferase activity in the microsomal fraction of the hamster heart and the enzyme activity in the cytosolic fraction was not affected. In contrast with the observations in rat hepatocytes, cytidylyltransferase from the hamster heart was not stimulated directly by stearic acid. The selective activation of the microsomal enzyme when the heart was perfused with stearic acid suggests that activation of the enzyme was mediated via the modification of the membrane by stearic acid.
Subject(s)
Fatty Acids, Nonesterified/pharmacology , Myocardium/metabolism , Phosphatidylcholines/biosynthesis , Animals , Arachidonic Acid , Arachidonic Acids/pharmacology , Biological Transport/drug effects , Choline/metabolism , Choline-Phosphate Cytidylyltransferase , Cricetinae , In Vitro Techniques , Kinetics , Mesocricetus , Nucleotidyltransferases/metabolism , Oleic Acid , Oleic Acids/pharmacology , Stearic Acids/pharmacologyABSTRACT
Myocardial ischemia was produced in the left ventricle of the canine heart by a Harris two-stage occlusion of the left anterior descending coronary artery. The lipid content in the ischemic myocardium was analyzed and compared with the control tissue. No significant change in total phospholipid and cholesterol was detected. A 2-fold elevation in the levels of the major lysophospoholipids was observed during acute ventricular arrhythmias at 24 hr after the onset of ischemia. Such increases were not caused by preferential hydrolysis of phospholipid plasmalogens from the parent phospholipids.