title: Benefits of perfusion preservation in canine hearts stored for short intervals.
abstract: BACKGROUND
  Continuous perfusion of donor hearts for transplantation has been proposed to improve graft function or extend preservation intervals, but the effects on cellular metabolism, myocyte loss, and myocardial edema are not well-defined.
  
  
  METHODS
  Hearts from mongrel dogs were instrumented with sonomicrometry crystals and left ventricular (LV) catheters. LV function was quantified by the preload-recruitable stroke work (PRSW) relationship. Hearts were arrested with a modified Celsior solution, and stored in cold solution (n=6) or placed in a device providing continuous perfusion of this solution at 10 mL/100 g/min (n=6). After 4 h of storage, left atrial samples were frozen, extracted, and analyzed by magnetic resonance spectroscopy (MRS). Hearts were then transplanted into recipient dogs and reperfused for 6 h with function measured hourly. At end-experiment, LV specimens were assayed for water content and apoptosis. Serum CK-MB levels were measured.
  
  
  RESULTS
  LV functional recovery was excellent in both groups over 6 h of reperfusion. MRS revealed a dramatic decrease in tissue lactate in hearts protected with continuous perfusion (P<0.01). Apoptotic cell counts were significantly lower in post-reperfusion heart tissue in animals undergoing a continuous perfusion strategy (P<0.01). CK-MB levels and LV water content were similar in both groups.
  
  
  CONCLUSIONS
  Although both methods of preservation lead to good early graft function after 4 h of protected ischemia, continuous preservation dramatically reduces tissue lactate accumulation without increasing myocardial edema and may reduce tissue damage during storage and reperfusion. It appears promising as a method to improve results of cardiac transplantation.
authors.affiliation: Department of Cardiovascular and Thoracic Surgery and the Advanced Imaging Research Center, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-8879, USA.
authors.forename: David H
authors.initials: DH
authors.lastname: Rosenbaum
authors.forename: Matthias
authors.initials: M
authors.lastname: Peltz
authors.forename: Matthew E
authors.initials: ME
authors.lastname: Merritt
authors.forename: Jeffrey E
authors.initials: JE
authors.lastname: Thatcher
authors.forename: Hideki
authors.initials: H
authors.lastname: Sasaki
authors.forename: Michael E
authors.initials: ME
authors.lastname: Jessen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D004285:Dogs; D004489:Edema, Cardiac / Q000473:pathology / Q000517:prevention & control; D006085:Graft Survival / Q000502:physiology; D006321:Heart / Q000502:physiology*; D016027:Heart Transplantation / Q000379:methods*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009336:Necrosis / Q000473:pathology / Q000517:prevention & control; D009926:Organ Preservation / Q000379:methods*; D010477:Perfusion / Q000379:methods*; D011897:Random Allocation; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology