Changes in fatty acid compositions of myocardial lipids in rats with heart failure following myocardial infarction.
Changes in fatty acid composition of myocardial lipids were examined in rats with heart failure following myocardial infarction. Left ventricular systolic pressure (LVSP) was decreased and left ventricular end-diastolic pressure (LVEDP) was elevated 24 h, 1 and 12 weeks after left coronary artery ligation (CAL), suggesting the development of heart failure at these periods in this model. Hearts were isolated 24 h, 1 week and 12 weeks after the operation. Myocardial lipids in the infarcted scar tissue, non-infarcted remaining left ventricle including interseptum and right ventricle were separated into phospholipid (PL), triacylglycerol (TG), diacylglycerol (DAG) and free fatty acid (FFA) fractions. In the scar tissue PL content markedly decreased whereas TG, DAG and FFA contents increased 24 h after CAL. Despite a marked decrease in constituted fatty acids of PL fraction in the scar tissue the percentage of arachidonic acid in PL was elevated 12 weeks after CAL, suggesting that release of arachidonic acid during PL degradation was suppressed. In the non-infarcted viable left ventricle PL content remained unchanged throughout the experiment whereas TG, DAG and FFA contents were elevated 24 h after CAL. Despite no changes in PL and other lipid contents in the non-infarcted tissue the percentage of linoleic acid in PL was reduced and that of docosahexaenoic acid in PL was elevated 12 weeks after CAL. Our findings showed that myocardial lipid composition of the non-infarcted left ventricle was altered only in an early stage of the development of heart failure and fatty acid compositions of PL was exchanged in a late stage of the development of heart failure. The exchange may be related to cardiac dysfunction or myocardial remodelling in the rat with heart failure.
Nasa
Y
Y
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
Sakamoto
Y
Y
Sanbe
A
A
Sasaki
H
H
Yamaguchi
F
F
Takeo
S
S
D000818:Animals; D004075:Diglycerides / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000032:analysis*; D006333:Heart Failure / Q000378:metabolism*; D006352:Heart Ventricles / Q000737:chemistry; D006439:Hemodynamics / Q000502:physiology; D008026:Ligation; D008297:Male; D008563:Membrane Lipids / Q000032:analysis*; D009203:Myocardial Infarction / Q000378:metabolism*; D010743:Phospholipids / Q000737:chemistry / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000378:metabolism
D004075:Diglycerides; D005230:Fatty Acids, Nonesterified; D008563:Membrane Lipids; D010743:Phospholipids; D014280:Triglycerides