title: Increased temperature reduces the protective effect of University of Wisconsin solution in the heart.
abstract: BACKGROUND
  The protective effect of University of Wisconsin solution (UW) for hypothermic storage of donor hearts has been demonstrated in the laboratory. However, clinical usage is associated with occasional primary graft failures. We postulated that this could be related to adverse effects of UW on the coronary vasculature during cardiac implantation and rewarming. We therefore assessed recovery of contractile function and coronary flow in rat hearts after cardioplegic arrest using UW compared with St. Thomas' solution (ST) at 4 degrees C or 25 degrees C.
  
  
  METHODS
  Cardioplegia was induced in isolated rat hearts using either UW or ST at 4 degrees C. Hearts were then maintained at 4 degrees C or 25 degrees C. In some hearts, UW at 4 degrees C was used for inducing arrest followed by flushing with ST at 4 degrees C and then rewarming to 25 degrees C. After 40 minutes of arrest, recovery of function and coronary flow were measured. Nuclear track emulsion was used to assess microvascular competence.
  
  
  RESULTS
  Compared with ST-treated hearts, UW-treated hearts showed significant reduction in recovery of function at 25 degrees C (76.2% +/- 4.0% versus 25.0% +/- 4.1%; p < 0.01) but not at 4 degrees C (88.0% +/- 1.6% versus 87.1% +/- 2.6%). Recovery of coronary flow in the UW-treated hearts at 25 degrees C was significantly lower than that in the ST-treated hearts at 25 degrees C (71.7% +/- 3.0% versus 94.5% +/- 6.3%; p < 0.01). At 25 degrees C, microvascular competence was reduced in the UW group compared with the ST group. At 25 degrees C, flushing out UW with ST resulted in greater recovery of function compared with UW throughout (73.4% +/- 7.1% versus 25.0% +/- 4.1%; p < 0.01).
  
  
  CONCLUSIONS
  University of Wisconsin solution provides effective donor heart protection under hypothermic conditions but can be deleterious at warmer temperatures.
authors.affiliation: Cardiac Surgical Research Unit, Baker Medical Research Institute and Alfred Hospital, Melbourne, Victoria, Australia.
authors.forename: R
authors.initials: R
authors.lastname: Ou
authors.forename: J B
authors.initials: JB
authors.lastname: Gavin
authors.forename: D S
authors.initials: DS
authors.lastname: Esmore
authors.forename: F L
authors.initials: FL
authors.lastname: Rosenfeldt
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology; D005978:Glutathione / Q000494:pharmacology; D006324:Heart Arrest, Induced; D016027:Heart Transplantation / Q000473:pathology / Q000502:physiology*; D007036:Hypothermia, Induced; D007328:Insulin / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008833:Microcirculation / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D009206:Myocardium / Q000473:pathology; D019188:Organ Preservation Solutions; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011189:Potassium Chloride / Q000494:pharmacology; D011887:Raffinose / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D013696:Temperature
chemical_list: D001639:Bicarbonates; D002314:Cardioplegic Solutions; D007328:Insulin; D019188:Organ Preservation Solutions; C041711:St. Thomas' Hospital cardioplegic solution; C055206:University of Wisconsin-lactobionate solution; D012965:Sodium Chloride; D000493:Allopurinol; D011189:Potassium Chloride; D005978:Glutathione; D008274:Magnesium; D000241:Adenosine; D002122:Calcium Chloride; D011887:Raffinose