title: Preservation of high-energy phosphate reserves in a cat model of post-ischemic myocardial dysfunction.
abstract: Brief episodes of myocardial ischemia are known to cause reversible depression of regional myocardial contraction after reperfusion. One of the mechanisms of this persistent regional dysfunction has been proposed to be depletion of high-energy phosphate compounds. Eight cats were prepared with a reversible snare occluder around the left anterior descending artery (LAD); a surface coil sutured to the epicardial surface over the LAD territory for measurement of 31-phosphorus (31P) magnetic resonance spectroscopy (MRS) spectra; and a pair of ultrasonic crystals implanted in the mid-myocardium for measurement of regional segment length shortening. The baseline value of percent segment length shortening (%SS) was 12.8 +/- 1.4%. Increased afterload did not significantly alter high-energy phosphate levels or %SS. All animals exhibited passive systolic bulging during occlusion (-8.4 +/- 3.6% systolic shortening) as well as reduced phosphocreatine (PRc, 30 +/- 3% of control) and increased inorganic phosphorus (Pi) (239 +/- 18%), but there was no change in adenosine triphosphate (ATP). During reflow, %SS did not completely recover (4.0 +/- 2.9%, P less than .05 versus baseline). PCr and Pi returned to control levels during the first 30 minutes of reperfusion. Increased afterload had no significant effect on high-energy phosphates or %SS in stunned hearts. These findings indicate a lack of correlation between recovery of high-energy phosphate stores and regional myocardial contractility in stunned myocardium. High-energy phosphate reserves are preserved in stunned myocardium and are unlikely to be a direct cause of myocardial dysfunction.
authors.affiliation: Department of Radiology, University of California, San Francisco 94143.
authors.forename: M
authors.initials: M
authors.lastname: Saeed
authors.forename: M F
authors.initials: MF
authors.lastname: Wendland
authors.forename: S
authors.initials: S
authors.lastname: Wagner
authors.forename: N
authors.initials: N
authors.lastname: Derugin
authors.forename: C B
authors.initials: CB
authors.lastname: Higgins
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002415:Cats; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D004734:Energy Metabolism / Q000502:physiology*; D009682:Magnetic Resonance Spectroscopy; D009200:Myocardial Contraction / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism*; D013997:Time Factors
chemical_list: D010710:Phosphates