Effect of Celsior and University of Wisconsin solutions on myocardial metabolism and function after warm ischemia.
BACKGROUND
Optimal preservation of donor hearts remains a significant concern during transplantation. Organ shortage led to an increase in the use of damaged hearts.


METHODS
To study the effect of preservation solutions on recovery of myocardial metabolism and function after warm ischemia, 10 dogs underwent 30 minutes of warm global ischemia under cardiopulmonary bypass. The animals were then administered 1 liter of Celsior (5 dogs), an extracellular crystalloid solution or 1 liter of University of Wisconsin solution (5 dogs), cooled at 4 degrees C, followed by 60 minutes of cold preservation and 30 minutes of warm blood reperfusion. Interstitial myocardial pH and pO2 changes were measured. The left ventricle dP/dt was measured before and after the ischemic episode, as where creatine kinase, troponine T and lactate serum levels.


RESULTS
Tissue pH averaged 6.9+/-0.1, 6.2+/-0.1, 6.7+/-0.1 and 6.8+/-0.1 before and after warm ischemia, following the 60 minutes of cold preservation and the reperfusion period in animals treated with the Celsior solution, compared to 6.8+/-0.1, 6.4+/-0.1, 7+/-0.1 and 6.8+/-0.2 respectively in dogs treated with the University of Wisconsin solution (p<0.05). Oxygen tension in the myocardium averaged 36+/-8 mmHg before warm ischemia and 59+/-31 mmHg after in animals that received Celsior compared to 30+/-10 mmHg and 49+/-7 mmHg in dogs treated with University of Wisconsin (p>0.05). Global myocardial function decreased significantly following reperfusion compared to baseline in both groups of animals. The serum levels of creatine kinase, troponine T and lactate increased significantly during the experiment although there was no significant difference between the 2 groups.


CONCLUSIONS
Both preservation solutions (Celsior and University of Wisconsin) resulted in suboptimal recovery of myocardial function and metabolism when administered after a period of warm ischemia. Strategies to improve recovery of damaged donor hearts remain to be appropriately defined.
Carrier
M
M
Cardiovascular Division, Montreal Heart Institute, Quebec, Canada.
Trudel
S
S
Pelletier
L C
LC
D000136:Acid-Base Equilibrium / Q000187:drug effects; D000241:Adenosine / Q000494:pharmacology; D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D005978:Glutathione / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D019344:Lactic Acid / Q000097:blood; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009926:Organ Preservation; D019188:Organ Preservation Solutions / Q000494:pharmacology*; D017680:Potassium Compounds / Q000494:pharmacology*; D011887:Raffinose / Q000494:pharmacology; D013696:Temperature; D020107:Troponin T / Q000097:blood; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
D007328:Insulin; D019188:Organ Preservation Solutions; D017680:Potassium Compounds; D020107:Troponin T; C055206:University of Wisconsin-lactobionate solution; C018369:potassium cardioplegic solution; D019344:Lactic Acid; D000493:Allopurinol; D003402:Creatine Kinase; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose