title: Enhancement of hypothermic heart preservation with fructose 1, 6-diphosphate.
abstract: BACKGROUND
  We hypothesized that the addition of fructose 1, 6-diphosphate (FDP) to a hypothermic heart preservation solution could improve metabolic recovery because it has several beneficial effects.
  
  
  METHODS
  Twenty adult Sprague-Dawley rats were used to study hypothermic heart preservation. The hearts were removed under general anesthesia and preserved at 4 degrees C in Euro-Collins solution (30 ml/kg) for 8 h. In the study group (N = 10), FDP (5 mM) was added to the Euro-Collins solution. In the control group (N = 10), no FDP was added. Heart function was studied after preservation using a working heart model. The ability of various concentrations of fructose 1,6-phosphate to passively diffuse through an egg phosphatidylcholine multilamellar vesicle (MLV) membrane bilayer was examined.
  
  
  RESULTS
  Cardiac output ranged from 17.0 +/- 1.9 to 24.9 +/- 1.6 ml/min in the study group vs 2.0 +/- 1.0-12.3 +/- 1.7 ml/min for controls, average aortic flow was 10. 8 +/- 1.4 ml/min in the study group vs -1.3 +/- 1.6 ml/min for controls, and maximum LV generated power was 22.8 +/- 1.7 J/min vs 10.1 +/- 1.6 J/min for controls. Coronary flow, left ventricular stroke volume and stroke work, and myocardial oxygen consumption were much higher in the study group than in the control group. Coronary vascular resistance was lower in the study group than in the control group. Electron microscopic study indicated that many myocytes displayed patches of swollen mitochondria in the control group, but was rarely observed in the study group. The addition of 50 mM FDP caused substantial changes in MLV permeability. No dose of sucrose buffers outside the vesicles resulted in a significant changes of MLV permeability.
  
  
  CONCLUSIONS
  Our results indicate that the addition of FDP to Euro-Collins solution significantly improves hypothermic rat heart preservation, and FDP appeared to cross the membrane bilayer.
authors.affiliation: Department of Surgery, University of Louisville, Louisville, Kentucky, 40292, USA.
authors.forename: W
authors.initials: W
authors.lastname: Niu
authors.forename: F
authors.initials: F
authors.lastname: Zhang
authors.forename: W
authors.initials: W
authors.lastname: Ehringer
authors.forename: M
authors.initials: M
authors.lastname: Tseng
authors.forename: L
authors.initials: L
authors.lastname: Gray
authors.forename: S
authors.initials: S
authors.lastname: Chien
mesh_terms: D000818:Animals; D002317:Cardiovascular Agents / Q000493:pharmacokinetics / Q000494:pharmacology*; D015925:Cryopreservation; D005635:Fructosediphosphates / Q000493:pharmacokinetics / Q000494:pharmacology*; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008051:Lipid Bilayers / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D009926:Organ Preservation; D009929:Organ Size / Q000502:physiology; D010063:Ovum / Q000737:chemistry; D010101:Oxygen Consumption / Q000502:physiology; D010713:Phosphatidylcholines / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002317:Cardiovascular Agents; D005635:Fructosediphosphates; D008051:Lipid Bilayers; D010713:Phosphatidylcholines; C029063:fructose-1,6-diphosphate