Leakage of heart fatty acid binding protein with ischemia and reperfusion in the rat
Fatty acids and their metabolites have been implicated as a cause of myocardial damage during ischemia. Fatty acid binding protein (FABP), an abundant low molecular weight protein present in the cytosol of myocytes, has been postulated to be a key fatty acid carrier protein in the myocardium. Postul...
Saved in:
Published in | Journal of molecular and cellular cardiology Vol. 21; no. 6; pp. 577 - 583 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Kent
Elsevier Ltd
01.06.1989
Elsevier |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Fatty acids and their metabolites have been implicated as a cause of myocardial damage during ischemia. Fatty acid binding protein (FABP), an abundant low molecular weight protein present in the cytosol of myocytes, has been postulated to be a key fatty acid carrier protein in the myocardium. Postulating that loss of FABP during ischemia could cause an increase in unbound intracellular fatty acids contributing to myocardial damage, we measured plasma FABP levels during 60 min of myocardial ischemia followed by 60 min of reperfusion in the rat. Peak levels were seen 15 min after reperfusion. Plasma levels were higher with larger areas of myocardial ischemia (1720 ± 528 ng/ml vs. 216 ± 76 ng/ml with smaller areas,
P < 0.02). Tissue levels after 60 min of ischemia and 60 min of reperfusion were decreased by over 50%, (1.0 ± 0.3 mg FABP/g wet wt compared with 2.9 ± 0.4 mg FABP/g wet wt in normal myocardium,
P < 0.005). The data is consistent with the proposal that loss of FABP contributes to the myocardial damage associated with ischemia and reperfusion. Additional studies are needed to determine the exact role of FABP in the regulation of fatty acid metabolism in the heart. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-2828 1095-8584 |
DOI: | 10.1016/0022-2828(89)90823-7 |