Abstract
Sodium arachidonate (AA, 1.5 mg/kg) was injected into the coronary arteries in 16 rabbits. Arrhythmia, marked ST-T depression and apnea appeared in all cases, and 7 cases died within 10 min after the AA. Before the injection, the thromboxane B2 (TXB2) value was 1.2 ± 0.2 ng/ml (mean ± SE) and the 6-keto-PGF1α value was 2.1 ± 0.4 ng/ml. Three minutes after the AA, TXB2 values were 5.0 ± 1.1 in the surviving cases and 17.9 ± 6.5 ng/ml in the cases which died. 6-keto-PGF1α values were 47.7 ± 4.6 in the surviving cases and 248.5 ± 69.3 ng/ml in the cases which died. There occurred no deaths in 7 cases pretreated with aspirin (ASA) and in 11 cases pretreated with OKY-046 and 1581, which are specific inhibitors of TXA2 synthetase. TXB2 values did not change in the ASA and OKY groups after the AA injection. 6-keto-PGF1α values did not change in the ASA group and increased in the OKY group after the AA injection. Histological findings of the heart showed more remarkable ischemic changes in the non-pretreated group than in the ASA and OKY groups. These results suggest a role for TXA2 in sudden death. PGI2 production was extremely enhanced, suggesting the presence of a protective mechanism against thrombogenesis in vivo.
