title: The effect of high buffer cardioplegia and secondary cardioplegia on cardiac preservation and postischemic functional recovery: a 31P NMR and functional study in Langendorff perfused pig hearts.
abstract: High buffer cardioplegia may provide protection against ischemic damage by reducing the extent of intracellular acidosis. Secondary cardioplegia may improve postischemic recovery by restoration of high energy phosphates, ionic gradients, and intracellular pH. To test these hypotheses, pig hearts were arrested with high buffer (150 mM MOPS) cardioplegia or modified St. Thomas' solution II and then kept ischemic at 12 degrees C for 8 h. High energy phosphates and intracellular pH were followed during the period of ischemia, using 31P nuclear magnetic resonance spectroscopy, and functional recovery was followed during reperfusion. The hearts arrested by high buffer cardioplegia showed significantly higher intracellular pH than hearts preserved with St. Thomas' solution, but there were no significant differences in high energy phosphates. There were no significant differences in functional recovery. We found, however, that secondary cardioplegia abolished ventricular fibrillation, and resulted in improved functional recovery after 8 h of ischemic preservation compared with the hearts reperfused with Krebs-Henseleit solution alone. Our results suggest that despite attenuating the decreases in intracellular pH, high buffer cardioplegia does not improve recovery following 8 h of preservation at 12 degrees C. Secondary cardioplegia reduces the incidence of ventricular fibrillation and improves postischemic functional recovery of the myocardium.
authors.affiliation: Department of Physiology, Faculty of Medicine, University of Ottawa, Ont., Canada.
authors.forename: G H
authors.initials: GH
authors.lastname: Tian
authors.forename: G W
authors.initials: GW
authors.lastname: Mainwood
authors.forename: G P
authors.initials: GP
authors.lastname: Biro
authors.forename: K E
authors.initials: KE
authors.lastname: Smith
authors.forename: K W
authors.initials: KW
authors.lastname: Butler
authors.forename: D
authors.initials: D
authors.lastname: Lawrence
authors.forename: R
authors.initials: R
authors.lastname: Deslauriers
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D002021:Buffers; D002118:Calcium / Q000627:therapeutic use*; D002122:Calcium Chloride / Q000627:therapeutic use; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D003327:Coronary Disease / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control*; D015925:Cryopreservation / Q000379:methods; D004305:Dose-Response Relationship, Drug; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007424:Intracellular Fluid / Q000378:metabolism; D008274:Magnesium / Q000627:therapeutic use; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D009926:Organ Preservation / Q000379:methods; D010725:Phosphocreatine / Q000031:analogs & derivatives / Q000378:metabolism; D010758:Phosphorus; D011189:Potassium Chloride / Q000627:therapeutic use; D012965:Sodium Chloride / Q000627:therapeutic use; D013552:Swine
chemical_list: D001639:Bicarbonates; D002021:Buffers; D002314:Cardioplegic Solutions; C041711:St. Thomas' Hospital cardioplegic solution; D010725:Phosphocreatine; D010758:Phosphorus; D012965:Sodium Chloride; C025403:phosphocreatinine; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D008274:Magnesium; D002122:Calcium Chloride; D002118:Calcium