title: Severity of lethal ischemia/reperfusion injury in rat hearts subjected to ischemic preconditioning is increased under conditions of simulated hyperglycemia.
abstract: The aim of our study was to characterize resistance to ischemia/reperfusion (I/R) injury in Langendorff-perfused rat hearts and effectivity of ischemic preconditioning (PC) under condition of simulated acute hyperglycemia (SAHG) by perfusion of the hearts with Krebs-Henseleit (KH) solution with elevated glucose concentration (22 mmol/l). I/R injury was induced by 30-min coronary occlusion followed by 120-min reperfusion and PC by two cycles of 5-min occlusion/5-min reperfusion, prior to I/R. The severity of I/R injury was characterized by determination of the size of infarction (IS, expressed in % of area at risk size) and the amount of heart-type fatty acid binding protein (h-FABP, a marker of cell injury) released from the hearts to the effluent. Significantly smaller IS (8.8+/-1 %) and lower total amount of released h-FABP (1808+/-660 pmol) in PC group compared with IS 17.1+/-1.2 % (p<0.01) and amount of h-FABP (8803+/-2415 pmol, p<0.05) in the non-PC control hearts perfused with standard KH solution (glucose 11 mmol/l) confirmed protective effects of PC. In contrast, in SAHG groups, PC enhanced IS (21.4+/-2.2 vs. 14.3+/-1.3 %, p<0.05) and increased total amount of h-FABP (5541+/-229 vs. 3458+/-283 pmol, p<0.05) compared with respective non-PC controls. Results suggest that PC has negative effect on resistance of the hearts to I/R injury under conditions of elevated glucose in vitro.
authors.affiliation: Institute for Heart Research, Slovak Academy of Science, Bratislava, Slovak Republic. mzmzalesak@gmail.com.
authors.forename: M
authors.initials: M
authors.lastname: Zálešák
authors.forename: P
authors.initials: P
authors.lastname: Blažíček
authors.forename: D
authors.initials: D
authors.lastname: Pancza
authors.forename: V
authors.initials: V
authors.lastname: Ledvényiová
authors.forename: M
authors.initials: M
authors.lastname: Barteková
authors.forename: M
authors.initials: M
authors.lastname: Nemčeková
authors.forename: S
authors.initials: S
authors.lastname: Čarnická
authors.forename: A
authors.initials: A
authors.lastname: Ziegelhöffer
authors.forename: T
authors.initials: T
authors.lastname: Ravingerová
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications* / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: C509948:FABP3 protein, rat; D000074026:Fatty Acid Binding Protein 3; D050556:Fatty Acid-Binding Proteins; D005947:Glucose