title: Metabolic and functional consequences of blunted myocardial reactive hyperemia.
abstract: This study determined whether the rapidity of myocardial metabolic and contractile recovery after brief coronary occlusion depends upon the intensity of reactive hyperemia. We also tested the hypothesis that coronary flow rate modulates contractility after brief myocardial ischemia, independent of changes in phosphorus metabolites. Eight open-chest pigs were studied with phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy with 14 s time resolution. After a 29-s anterior descending coronary occlusion, peak Doppler coronary flow velocity was alternately unrestricted (normal hyperemia, 443 +/- 40% of control) or limited to 159 +/- 9% of control. During 29 s coronary occlusion, phosphocreatine-to-inorganic phosphate ratio (PCr/Pi) and systolic segment shortening in the ischemic region fell to 28 +/- 4 and 7 +/- 7% of control, respectively. With normal hyperemia, PCr/Pi and segment shortening recovered within 29 s. With blunted hyperemia, recovery of both parameters was delayed an additional 29-43 s, associated with reduced subendocardial blood flow (measured with radioactive microspheres) and persistent intracellular acidosis. However, the relationship between segment shortening and PCr/Pi was unaffected by the intensity of reactive hyperemia. Thus blunted reactive hyperemia significantly delays metabolic and contractile recovery from brief ischemia, probably via transient maldistribution of transmural perfusion. However, coronary blood flow rate does not independently modulate contractility after brief reversible ischemia.
authors.affiliation: Cardiology Section, Veterans Affairs Medical Center, San Francisco, California 94121.
authors.forename: G G
authors.initials: GG
authors.lastname: Schwartz
authors.forename: S
authors.initials: S
authors.lastname: Schaefer
authors.forename: S D
authors.initials: SD
authors.lastname: Trocha
authors.forename: S
authors.initials: S
authors.lastname: Steinman
authors.forename: J
authors.initials: J
authors.lastname: Gober
authors.forename: J
authors.initials: J
authors.lastname: Garcia
authors.forename: B
authors.initials: B
authors.lastname: Massie
authors.forename: M W
authors.initials: MW
authors.lastname: Weiner
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology* / Q000503:physiopathology; D004734:Energy Metabolism; D005260:Female; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006940:Hyperemia / Q000503:physiopathology*; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D009206:Myocardium / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D015424:Reperfusion; D013552:Swine; D013599:Systole; D013997:Time Factors
chemical_list: D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate