title: Adding bupivacaine to high-potassium cardioplegia improves function and reduces cellular damage of rat isolated hearts after prolonged, cold storage.
abstract: BACKGROUND
  Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone.
  
  
  METHODS
  After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 microm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4 degrees C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured.
  
  
  RESULTS
  All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P < 0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P < 0.001) but did not differ from baseline.
  
  
  CONCLUSIONS
  Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.
authors.affiliation: Department of Physiology and Biophysics, University of Illinois College of Medicine at Chicago, and Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA.
authors.forename: James D
authors.initials: JD
authors.lastname: Ross
authors.forename: Richard
authors.initials: R
authors.lastname: Ripper
authors.forename: William R
authors.initials: WR
authors.lastname: Law
authors.forename: Malek
authors.initials: M
authors.lastname: Massad
authors.forename: Patricia
authors.initials: P
authors.lastname: Murphy
authors.forename: Lucas
authors.initials: L
authors.lastname: Edelman
authors.forename: Beth
authors.initials: B
authors.lastname: Conlon
authors.forename: Douglas L
authors.initials: DL
authors.lastname: Feinstein
authors.forename: June W
authors.initials: JW
authors.lastname: Palmer
authors.forename: Guido
authors.initials: G
authors.lastname: DiGregorio
authors.forename: Guy L
authors.initials: GL
authors.lastname: Weinberg
mesh_terms: D000779:Anesthetics, Local / Q000494:pharmacology*; D000818:Animals; D002045:Bupivacaine / Q000494:pharmacology*; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003080:Cold Temperature; D005217:Fat Emulsions, Intravenous; D006321:Heart / Q000187:drug effects*; D006324:Heart Arrest, Induced; D006334:Heart Function Tests; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D019188:Organ Preservation Solutions / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014021:Tissue Preservation
chemical_list: D000779:Anesthetics, Local; D002314:Cardioplegic Solutions; D005217:Fat Emulsions, Intravenous; D019188:Organ Preservation Solutions; D007770:L-Lactate Dehydrogenase; D011188:Potassium; D002045:Bupivacaine