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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.

Additive protection of aprotinin, protease inhibitor to cold cardioplegia from ischemic myocardium.