title: Plasma and urinary heart-type cytoplasmic fatty acid-binding protein in coronary occlusion and reperfusion induced myocardial injury model.
abstract: The leakage of heart-type cytoplasmic fatty acid-binding protein (H-FABPc) from injured myocardial cells has been reported. We have previously proposed that its plasma and urinary levels could be used as an early indicator of myocardial injury and also reflect the severity of myocardial injury. To confirm this hypothesis, the time course of changes of the plasma and urinary H-FABPc was investigated during myocardial injury induced by coronary artery occlusion and reperfusion in dogs. The plasma elimination kinetics and urinary excretion kinetics of H-FABPc were also analysed in dogs which were given a bolus injection of exogenous H-FABPc. The distribution of circulating H-FABPc was determined in mice by whole-body autoradiography using 125I-labelled H-FABPc. In myocardial injury model, plasma and urinary H-FABPc level showed rapid increase after reperfusion. The elimination kinetic study revealed that H-FABPc was mono-exponentially cleared from the circulation. The elimination rate constant (Ke) was 0.0275 +/- 0.0094/min (mean +/- S.D., n = 7) and the disappearance half-time (t1/2) was 27.5 +/- 8.4 min (mean +/- S.D., n = 7). Exogenous H-FABPc appeared in urine soon after administration, with the peak level being at 6.9 +/- 2.0 min (mean +/- S.D., n = 7). Whole-body autoradiography also demonstrated that 125I-H-FABPc accumulated rapidly in the kidneys. This study demonstrated that H-FABPc leaked rapidly from injured myocardium and rapidly appeared in plasma and urine. Infarct size was closely correlated with the calculated H-FABPc release (r = 0.89, r2 = 0.80, P < 0.01, n = 7) and with the amount of the urinary H-FABPc (r = 0.94, r2 = 0.88, P < 0.01, n = 7). These data suggest that measurement of the H-FABPc levels in plasma and urine might be useful for the early detection of myocardial injury and also for the assessment of infarct size.
authors.affiliation: Department of Internal Medicine, Osaka Medical College, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sohmiya
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: R
authors.initials: R
authors.lastname: Tsuji
authors.forename: K
authors.initials: K
authors.lastname: Yoshimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Nakayama
authors.forename: Y
authors.initials: Y
authors.lastname: Hirota
authors.forename: K
authors.initials: K
authors.lastname: Kawamura
authors.forename: Y
authors.initials: Y
authors.lastname: Matsunaga
authors.forename: S
authors.initials: S
authors.lastname: Nishimura
authors.forename: H
authors.initials: H
authors.lastname: Miyazaki
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D050556:Fatty Acid-Binding Proteins; D005260:Female; D007527:Isoenzymes; D008657:Metabolic Clearance Rate; D009203:Myocardial Infarction / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000175:diagnosis / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009363:Neoplasm Proteins
chemical_list: D002352:Carrier Proteins; D050556:Fatty Acid-Binding Proteins; D007527:Isoenzymes; D009363:Neoplasm Proteins; D003402:Creatine Kinase