title: Ischemic contracture begins when anaerobic glycolysis stops: a 31P-NMR study of isolated rat hearts.
abstract: The relationships among myocardial ATP, intracellular pH, and ischemic contracture in Langendorff-perfused rat hearts were investigated by 31P nuclear magnetic resonance spectroscopy during total global normothermic ischemia while the left ventricular pressure was recorded continuously via an intraventricular balloon. Glucose-perfused hearts (n = 63) were divided into five groups based on the time of onset of contracture (TOC), and three other groups of hearts were treated to vary the ischemic glycogen availability. ATP levels, which showed no evidence of accelerated ATP depletion during contracture, were significant and variable at TOC. Intracellular pH initially declined and then leveled off at TOC, with lower final pH in hearts with later TOC. We conclude that contracture began when anaerobic glycolysis (and thus glycolytic ATP synthesis) stopped. These results, though consistent with the concept that ischemic contracture in normal hearts results from rigor bond formation due to low ATP levels at the myofibrils, suggest that TOC is more closely related to glycolytic ATP production than to total cellular ATP content, thus providing evidence of some degree of subcellular compartmentation or metabolite channeling. In glycolytically inhibited hearts, the quite early contracture may have a Ca2+ component.
authors.affiliation: Gray Freshwater Biological Institute, University of Minnesota, Navarre 55392.
authors.forename: P B
authors.initials: PB
authors.lastname: Kingsley
authors.forename: E Y
authors.initials: EY
authors.lastname: Sako
authors.forename: M Q
authors.initials: MQ
authors.lastname: Yang
authors.forename: S D
authors.initials: SD
authors.lastname: Zimmer
authors.forename: K
authors.initials: K
authors.lastname: Ugurbil
authors.forename: J E
authors.initials: JE
authors.lastname: Foker
authors.forename: A H
authors.initials: AH
authors.lastname: From
mesh_terms: D000693:Anaerobiosis; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D006003:Glycogen / Q000378:metabolism; D006019:Glycolysis; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus; D051381:Rats; D013997:Time Factors
chemical_list: D010725:Phosphocreatine; D010758:Phosphorus; D006003:Glycogen