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

1980; Japanese Circulation Society; Volume: 44; Issue: 10 Linguagem: Inglês

10.1253/jcj.44.771

1347-4839

Makoto Sunamori, Jun Amano, Takaaki Kameda, Takao Okamura, Masayoshi Ozeki, Akio Suzuki,

Metabolomics and Mass Spectrometry Studies

Protective action of aprotinin from 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 280°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 nontreated 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 .