title: Early reperfusion with warm, polarizing adenosine-lidocaine cardioplegia improves functional recovery after 6 hours of cold static storage.
abstract: OBJECTIVE
  Rewarming and reanimating the donor heart from cold static storage predisposes the organ to injury and graft dysfunction. Our main aim was to investigate the effects of 5 minutes of continuous rewarming with a normokalemic, oxygenated, polarizing adenosine-lidocaine arrest solution after 6 hours of cold static storage (4°C) in adenosine-lidocaine or Celsior (Genzyme Corp, Cambridge, Mass) solutions.
  
  
  METHODS
  Male Sprague-Dawley rats (350-450 g, n = 40) were randomly assigned to one of 5 groups: (1) adenosine-lidocaine cold arrest with modified Krebs-Henseleit rewarming, (2) adenosine-lidocaine cold arrest with adenosine-lidocaine rewarming, (3) Celsior cold arrest with Celsior rewarming, (4) Celsior cold arrest with Krebs-Henseleit, and (5) Celsior cold arrest with adenosine-lidocaine arrest rewarming. Hearts were perfused in working mode, arrested (37°C), removed and stored for 6 hours at 4°C, reattached in Langendorff mode, and rewarmed for 5 minutes (37°C). Hearts were switched to working mode, and function was compared with prestorage values. Myocardial oxygen consumption and effluent lactate and pH values were measured during rewarming and recovery.
  
  
  RESULTS
  Cold adenosine-lidocaine hearts rewarmed with Krebs-Henseleit recovered 40% aortic flow and 58% coronary flow at 60 minutes of reperfusion. Rewarming with adenosine-lidocaine arrest solution led to significantly higher aortic flow (63%) and coronary flow (77%) at 60 minutes. Cold Celsior hearts rewarmed with Celsior had 9 times higher effluent lactate values with acidosis (pH 6.5) during the last minute of rewarming compared with all groups, and this was associated with early myocardial, vascular, and electrical stunning. At 5 and 10 minutes of recovery, the aortic flow was 1.0 and 8 mL/min, respectively. If cold Celsior hearts were rewarmed with adenosine-lidocaine, they generated 18-fold higher aortic flow and 16-fold higher coronary flow at 5 minutes. At 60 minutes, cold Celsior with Celsior-rewarmed hearts recovered 35% aortic flow and 50% coronary flow compared with 44% aortic flow and 67% coronary flow (P < .05) for Celsior with adenosine-lidocaine-rewarmed hearts. Celsior with Krebs-Henseleit-rewarmed hearts recovered 39% aortic flow and 51% coronary flow and were not significantly different from Celsior-rewarmed hearts. The myocardial oxygen consumption in the last minute of rewarming was 1.6 times higher for cold adenosine-lidocaine hearts rewarmed with adenosine-lidocaine compared with cold Celsior and Celsior hearts (19 vs 12 μmol O(2)/min/g dry weight) along with low lactate values and no acidosis.
  
  
  CONCLUSIONS
  Rewarming the rat heart after cold static storage in polarizing adenosine-lidocaine arrest solution resulted in significantly higher aortic flow, coronary flow, and cardiac output compared with that seen after Krebs-Henseleit or Celsior rewarming. Rewarming cold Celsior hearts with adenosine-lidocaine solution reduced stunning. Adenosine-lidocaine cardioplegia might offer a new reperfusion strategy after cold static storage.
authors.affiliation: Heart Research Laboratory, Department of Physiology and Pharmacology, James Cook University, Townsville, Queensland, Australia.
authors.forename: Donna M
authors.initials: DM
authors.lastname: Rudd
authors.forename: Geoffrey P
authors.initials: GP
authors.lastname: Dobson
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000503:physiopathology; D001794:Blood Pressure; D002302:Cardiac Output; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D050377:Cold Ischemia / Q000009:adverse effects; D003326:Coronary Circulation; D004187:Disaccharides / Q000494:pharmacology; D004573:Electrolytes / Q000494:pharmacology; D005971:Glutamates / Q000494:pharmacology; D005978:Glutathione / Q000494:pharmacology; D006324:Heart Arrest, Induced / Q000379:methods*; D006339:Heart Rate; D016027:Heart Transplantation / Q000009:adverse effects; D006639:Histidine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000378:metabolism; D008012:Lidocaine / Q000494:pharmacology*; D008297:Male; D008353:Mannitol / Q000494:pharmacology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D012039:Regional Blood Flow; D013997:Time Factors; D052096:Warm Ischemia / Q000009:adverse effects
chemical_list: D002314:Cardioplegic Solutions; C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D019344:Lactic Acid; D008353:Mannitol; D006639:Histidine; D000255:Adenosine Triphosphate; D008012:Lidocaine; D005978:Glutathione; D000241:Adenosine