title: Relationship between myocardial metabolites and contractile abnormalities during graded regional ischemia. Phosphorus-31 nuclear magnetic resonance studies of porcine myocardium in vivo.
abstract: The mechanisms responsible for changes in myocardial contractility during regional ischemia are unknown. Since changes in high-energy phosphates during ischemia are sensitive to reductions in myocardial blood flow, it was hypothesized that myocardial function under steady-state conditions of graded regional ischemia is closely related to changes in myocardial high-energy phosphates. Therefore, phosphorus-31 nuclear magnetic resonance spectroscopy was employed in an in vivo porcine model of graded coronary stenosis. Simultaneous measurements of regional subendocardial blood flow, high-energy phosphates, pH, and myocardial segment shortening were made during various degrees of regional ischemia in which subendocardial blood flow was reduced by 16-94%. During mild reductions in myocardial blood flow (subendocardial blood flow = 83% of nonischemic myocardium), only the ratio of phosphocreatine to inorganic phosphate (PCr/Pi), Pi, and [H+] were significantly changed from control. PCr, ATP, and PCr/ATP were not significantly reduced from control with mild reductions in blood flow. Changes in myocardial segment shortening were most closely associated with changes in PCr/Pi (r = 0.94). Pi and [H+] were negatively correlated with segment shortening (r = -0.64 and -0.58, respectively) and increased over twofold when blood flow was reduced by 62%. Thus, these data demonstrate that PCr/Pi is sensitive to reductions in myocardial blood flow and closely correlates with changes in myocardial function. These data are also consistent with a role for Pi or H+ as inhibitors of myocardial contractility during ischemia.
authors.affiliation: Magnetic Resonance Unit, Veterans Administration Medical Center, San Francisco, California 94121.
authors.forename: S
authors.initials: S
authors.lastname: Schaefer
authors.forename: G G
authors.initials: GG
authors.lastname: Schwartz
authors.forename: J R
authors.initials: JR
authors.lastname: Gober
authors.forename: A K
authors.initials: AK
authors.lastname: Wong
authors.forename: S A
authors.initials: SA
authors.lastname: Camacho
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 / Q000378:metabolism* / Q000503:physiopathology; D004734:Energy Metabolism; D005260:Female; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D013552:Swine
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate