title: The role of magnesium in postischemic cardiac dysfunction.
abstract: BACKGROUND
  The biochemical basis for postischemic myocardial stunning is not fully elucidated. Magnesium is an important regulator of cellular energetic processes and excitation-contraction coupling. We hypothesized that the decrease in function in the postischemic period may be the result of an alteration in magnesium regulation.
  
  
  METHODS
  In a Langendorf perfused rabbit heart model, we used 31P nuclear magnetic resonance spectroscopy to noninvasively determine intracellular Mg2+ and high-energy phosphate levels in the preischemic period and after a 30-minute period of normothermic ischemia. We measured adenosine triphosphate (ATP), phosphocreatine, and the phosphocreatine/inorganic phosphate ratio and calculated the free energy of ATP hydrolysis (delta GATP). On reperfusion, hearts were divided into three groups (n = 7 per group)--those receiving unmodified Krebs-Henseleit (control), 192 ng/ml dobutamine, or 5 mmol/L pyruvate.
  
  
  RESULTS
  Function (expressed as the rate-pressure product) was approximately 77% of preischemic values in the control group, whereas in both dobutamine and pyruvate groups it returned to preischemic levels. ATP was decreased similarly in all groups in the postischemic period. Phosphocreatine/inorganic phosphate ratio and delta GATP were higher in the pyruvate group compared with the other groups. Intracellular Mg2+ was elevated significantly in the unmodified control postischemic group compared with preischemic, postischemic dobutamine, and pyruvate groups (1.0 +/- 0.12 vs 0.80 +/- 0.08, 0.64 +/- 0.08, and 0.70 +/- 0.05 mmol/L, respectively; p less than 0.05).
  
  
  CONCLUSIONS
  We conclude that (1) postischemic "stunned" hearts have elevated Mg2+ levels in association with impaired contractile function, (2) inotropic agents improve contractile function in association with a decline in Mg2+ to preischemic levels despite differing effects on intracellular energetics, and (3) Mg2+ may play an important regulatory role in the heart after ischemia.
authors.affiliation: Division of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, PA 15213.
authors.forename: K E
authors.initials: KE
authors.lastname: Sommers
authors.forename: A
authors.initials: A
authors.lastname: Ohkado
authors.forename: E
authors.initials: E
authors.lastname: Simplaceanu
authors.forename: A P
authors.initials: AP
authors.lastname: Koretsky
authors.forename: C
authors.initials: C
authors.lastname: Ho
authors.forename: P J
authors.initials: PJ
authors.lastname: del Nido
mesh_terms: D000818:Animals; D002851:Chromatography, High Pressure Liquid; D004734:Energy Metabolism; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology*; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D010710:Phosphates / Q000378:metabolism; D010758:Phosphorus; D011817:Rabbits
chemical_list: D010710:Phosphates; D010758:Phosphorus; D008274:Magnesium