title: Arrhythmia after the release of inhibited oxidative phosphorylation.
abstract: Automaticities due to delayed afterdepolarizations, elicited upon reoxygenation, are thought to be caused by Ca overload. Since tissue Ca uptake upon reoxygenation has been reported to be closely related to metabolic inhibition during hypoxic perfusion, the relationship between the degree of metabolic inhibition during hypoxia and reoxygenation-induced arrhythmias was investigated in guinea pig papillary muscles. (1) Arrhythmias occurred after 60 min substrate-free hypoxia, but not after 30 min hypoxia. The chance of automaticities was closely related with the increase in resting tension achieved during hypoxic period. The incidence of arrhythmias was, however, lower after 90 or 120 min hypoxia. (2) There were arrhythmias after 20-30 min hypoxia with glycolytic inhibition (20 mM 2-deoxyglucose + 5 mM acetate). On the other hand, 60-min hypoxia in the presence of 5 mM glucose did not elicit arrhythmias on reoxygenation. (3) Stimulation of glycolysis (50 mM glucose) during substrate-free hypoxia prolonged the action potential duration, but did not cause arrhythmias. Washout of cyanide (1 mM) after 60 min perfusion in the presence of oxygen, caused arrhythmias and aftercontractions. These results suggest that the degree of metabolic inhibition during hypoxia is closely related to Ca overload and the resultant arrhythmias upon reoxygenation. The release of inhibited oxidative phosphorylation, rather than the reintroduction of oxygen per se, was thought to be the key mechanism of reoxygenation-induced arrhythmias.
authors.affiliation: Third Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Terada
authors.forename: A
authors.initials: A
authors.lastname: Kobayashi
authors.forename: N
authors.initials: N
authors.lastname: Yamazaki
authors.forename: T F
authors.initials: TF
authors.lastname: McDonald
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D003327:Coronary Disease / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D004594:Electrophysiology; D006019:Glycolysis; D006168:Guinea Pigs; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D010084:Oxidation-Reduction / Q000187:drug effects; D010100:Oxygen / Q000378:metabolism; D010210:Papillary Muscles / Q000378:metabolism / Q000503:physiopathology; D010766:Phosphorylation / Q000187:drug effects; D012966:Sodium Cyanide / Q000494:pharmacology
chemical_list: D012966:Sodium Cyanide; D010100:Oxygen