title: Superior myocardial preservation with HTK solution over Celsior in rat hearts with prolonged cold ischemia.
abstract: BACKGROUND
  Increasing allograft ischemic time is a significant risk factor for mortality following heart transplantation (HTx). The purpose of this study was to evaluate the protective effects of histidine-tryptophan-ketoglutarate (HTK) and Celsior (CEL) using a rat HTx model with prolonged cold storage.
  
  
  METHODS
  The hearts were excised from donor rats, stored in cold preservation solution for either 6 or 18 hours, and heterotopically transplanted into syngeneic recipients. Serum creatine phosphokinase (CPK), serum troponin I, graft-infiltrating cells, graft mRNA levels for inflammatory mediators, and tissue adenosine triphosphate (ATP) levels were analyzed, as markers of graft injury.
  
  
  RESULTS
  The recipients of grafts stored in HTK for 18 hours of prolonged cold ischemia had lower levels of serum CPK and tissue malondialdehyde, less upregulation of the mRNAs for IL-6 and inducible nitric oxide synthase, less apoptosis, and higher ATP levels than those receiving grafts stored in CEL and Saline. Cardiac contraction 3 hours after reperfusion was observed in 43% of the cardiac grafts stored in HTK for 18 hours, while no cardiac wall movement was seen in grafts stored in either saline or CEL.
  
  
  CONCLUSIONS
  Cold storage in HTK exhibited superior protective effects against prolonged cold ischemia in a syngeneic rat transplantation model.
authors.affiliation: The Heart, Lung and Esophageal Surgery Institute, University of Pittsburgh, Pittsburgh, PA, USA.
authors.forename: Sungsoo
authors.initials: S
authors.lastname: Lee
authors.forename: Chien-Sheng
authors.initials: CS
authors.lastname: Huang
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Kawamura
authors.forename: Norihisa
authors.initials: N
authors.lastname: Shigemura
authors.forename: Donna B
authors.initials: DB
authors.lastname: Stolz
authors.forename: Timothy R
authors.initials: TR
authors.lastname: Billiar
authors.forename: James D
authors.initials: JD
authors.lastname: Luketich
authors.forename: Atsunori
authors.initials: A
authors.lastname: Nakao
authors.forename: Yoshiya
authors.initials: Y
authors.lastname: Toyoda
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D050377:Cold Ischemia; D003402:Creatine Kinase / Q000097:blood; D004187:Disaccharides; D004573:Electrolytes; D005947:Glucose; D005971:Glutamates; D005978:Glutathione; D006321:Heart; D016027:Heart Transplantation / Q000473:pathology / Q000502:physiology; D006639:Histidine; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008353:Mannitol; D046529:Microscopy, Electron, Transmission; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D009504:Neutrophils / Q000473:pathology; D009926:Organ Preservation / Q000379:methods*; D019188:Organ Preservation Solutions; D011189:Potassium Chloride; D011343:Procaine; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D019210:Troponin I / Q000097:blood
chemical_list: C039984:Bretschneider cardioplegic solution; C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D018836:Inflammation Mediators; D019188:Organ Preservation Solutions; D012333:RNA, Messenger; D019210:Troponin I; D008353:Mannitol; D006639:Histidine; D011343:Procaine; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D055372:AMP-Activated Protein Kinases; D003402:Creatine Kinase; D005978:Glutathione; D005947:Glucose