title: The effect of lactate infusion on myocardial metabolism and ventricular function following ischemia and cardioplegia.
abstract: Impaired myocardial fatty acid and glucose metabolism following ischemia and cardioplegia may limit the recovery of myocardial oxidative metabolism and ventricular function. Lactate, a simple three carbon compound, can be readily metabolized to pyruvate and is possibly the preferred substrate for aerobic metabolism. Therefore, increasing arterial lactate concentrations may improve myocardial metabolic recovery after ischemia and cardioplegia. Myocardial lactate metabolism and ventricular function were assessed in a canine model of 45 mins of global normothermic ischemia followed by 60 mins of cold potassium cardioplegic arrest. Thirteen dogs received a perioperative infusion of sodium lactate to elevate arterial concentrations (from 6 to 12 mmol/L) and 12 dogs received an equivalent amount of saline. The high arterial lactate concentrations were associated with an increased myocardial lactate consumption and oxidation (as assessed by 14C-labelled lactate) during reperfusion. Myocardial ATP concentrations fell during reperfusion despite improved myocardial oxidation. The recovery of ventricular function (as assessed by a compliant intraventricular balloon) was incomplete and only marginally better with the high arterial lactate concentrations. An infusion of lactate improved myocardial oxidative metabolism following ischemia and cardioplegia. However, the recovery of ventricular function was incomplete perhaps because of inadequate preservation of myocardial ATP.
authors.affiliation: Division of Cardiovascular Surgery, Toronto General Hospital, Ontario.
authors.forename: K H
authors.initials: KH
authors.lastname: Teoh
authors.forename: D A
authors.initials: DA
authors.lastname: Mickle
authors.forename: R D
authors.initials: RD
authors.lastname: Weisel
authors.forename: M M
authors.initials: MM
authors.lastname: Madonik
authors.forename: J
authors.initials: J
authors.lastname: Ivanov
authors.forename: R D
authors.initials: RD
authors.lastname: Harding
authors.forename: A D
authors.initials: AD
authors.lastname: Romaschin
authors.forename: G J
authors.initials: GJ
authors.lastname: Wilson
authors.forename: J C
authors.initials: JC
authors.lastname: Mullen
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery; D004195:Disease Models, Animal; D004285:Dogs; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006324:Heart Arrest, Induced; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics; D007262:Infusions, Intravenous; D007773:Lactates / Q000378:metabolism / Q000494:pharmacology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D010725:Phosphocreatine / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D005947:Glucose