Additive protection of aprotinin, protease inhibitor to cold cardioplegia from ischemic myocarium.
Protective action of aprotinin froom ischemic myocardial damage was evaluated in 9 patients compared to non-treated 18 patients, who underwent open heart surgery (22 ACB, 3 AVR and 2 MVR) with respect to the alterations of beta-glucronidase, acid-phosphatase, MB-CPK and m-GOT. Cold cardioplegia with glucose-insulin-potassium solution was used in this investigation. Average arrest time was 78.6 +/- 4.9 minutes associated with hypothermia between 25 and 28 degrees C in rectal temperature. Aprotinin was administered in 9 patients intravenously with 5,000 KIU/Kg 30 minutes prior to CPB and then 5,000 KIU/Kg in the prime solution. Activity of beta-glucronidase was significantly suppressed in the aprotinin-treated group compared to the non-treated group following cardioplegia and in the reperfusion period up to 6 hours, however, acid-phosphatase failed to demonstrate significant difference among two groups. Serum MB-CPK and m-GOT levels in the aprotinin-treated group did not elevate the beginning of reperfusion following cardioplegia. These data suggest that aprotinin add myocardial protection to cold cardioplegia.
D000135:Acid Phosphatase / Q000032:analysis; D007611:Aprotinin / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D003327:Coronary Disease / Q000517:prevention & control*; D003402:Creatine Kinase / Q000097:blood; D006324:Heart Arrest, Induced; D006801:Humans; D007036:Hypothermia, Induced; D007527:Isoenzymes; D008247:Lysosomes / Q000201:enzymology
D007527:Isoenzymes; D007611:Aprotinin; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D000135:Acid Phosphatase