Effect of aprotinin to improve myocardial viability in myocardial preservation followed by reperfusion.
Isolated canine hearts were preserved at 4 degrees C with multi-dose cardioplegic solution every hour for 6 hours. Reperfusion was observed for 2 hours under cross-circulation without cardiotonic drugs. The aprotinin group (n = 8), which received cardioplegic solution with added aprotinin (150 KIU/mL), was compared with the control group (n = 6). The increase in tissue adenosine triphosphate and total adenine nucleotide content during reperfusion was significant in the aprotinin group; there was no change in the control group, and the levels at the end of reperfusion tended to be higher in the aprotinin group than in the control group. Tissue adenosine diphosphate levels remained unchanged in both groups. Tissue adenosine monophosphate levels declined during reperfusion in both groups and were slightly lower in the control group. Tissue levels of cyclic adenosine monophosphate remained unchanged in the aprotinin group whereas they increased during ischemia and declined significantly during reperfusion in the control group. Tissue levels of cyclic guanosine monophosphate declined during reperfusion in both groups without difference. Creatine phosphate levels recovered in both groups without difference. Serum cyclic guanosine monophosphate concentration tended to be lower in the aprotinin group than in the control group. Serum creatine kinase-MB level increased slightly during reperfusion in both groups without difference. N-acetyl-beta-D-glucosaminidase levels were significantly suppressed during reperfusion in the aprotinin group as compared with the control group. These results suggest that aprotinin is effective in preserving adenine nucleotide and adenosine triphosphate levels and in stabilizing tissue cyclic adenosine monophosphate levels in prolonged hypothermic cardioplegic preservation followed by reperfusion.
Sunamori
M
M
Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, Japan.
Sultan
I
I
Suzuki
A
A
D000118:Acetylglucosaminidase / Q000378:metabolism; D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D007611:Aprotinin / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D004285:Dogs; D006324:Heart Arrest, Induced; D066298:In Vitro Techniques; D007527:Isoenzymes; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009926:Organ Preservation; D014022:Tissue Survival; D016277:Ventricular Function, Left
D000227:Adenine Nucleotides; D007527:Isoenzymes; D007611:Aprotinin; D000242:Cyclic AMP; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D000118:Acetylglucosaminidase