title: Involvement of energetic metabolism in the effects of ischemic postconditioning on the ischemic-reperfused heart of fed and fasted rats.
abstract: The effects of ischemic-postconditioning (IPOC) on functional recovery and cell viability of ischemic-reperfused hearts from fed and fasted rats were studied in relation to triacylglycerol and glycogen mobilization, ATP content, glucose-6-phosphate dehydrogenase activity and reduced/oxidized glutathione (GSH/GSSG). Oxidative damage was estimated by measuring thiobarbituric acid reactive substances (TBARS). IPOC improved contractile recovery and cell viability in the fed but attenuated them in the fasted hearts. In both groups ischemia lowered glycogen. IPOC further reduced it. Triacylglycerol remained unchanged during ischemia-reperfusion in both groups, but triacylglycerol mobilization was activated by IPOC in the fasted group. ATP was increased by IPOC in the fed hearts, but lowered in the fasted ones, which appeared to be associated with the rates of ATP synthesis in isolated mitochondria. In the fed hearts IPOC raised glucose-6-phosphate dehydrogenase activity and GSH/GSSG, and lowered TBARS. These results suggest that IPOC effects are associated with changes in the ATP supply, mobilization of energy sources and glutathione antioxidant ratio.
authors.affiliation: Physiology Unit, Department of Biological Sciences, School of Pharmacy and Biochemistry, University of Buenos Aires and IQUIMEFA-CONICET, Argentina.
authors.forename: M G
authors.initials: MG
authors.lastname: Marina Prendes
authors.forename: R
authors.initials: R
authors.lastname: Hermann
authors.forename: M E
authors.initials: ME
authors.lastname: Torresin
authors.forename: P
authors.initials: P
authors.lastname: Souto
authors.forename: S
authors.initials: S
authors.lastname: Tallis
authors.forename: E A
authors.initials: EA
authors.lastname: Savino
authors.forename: A
authors.initials: A
authors.lastname: Varela
authors.forename: M M
authors.initials: MM
authors.lastname: Jaitovich
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D005215:Fasting / Q000502:physiology*; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D057775:Ischemic Postconditioning; D008929:Mitochondria, Heart / Q000378:metabolism; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; C023010:4-hydroxyphenylglycine; D000255:Adenosine Triphosphate; D006003:Glycogen; D005954:Glucosephosphate Dehydrogenase; D005978:Glutathione; D005998:Glycine; D019803:Glutathione Disulfide