Yamazaki H, Isohisa I, Tanoue K
Jpn Circ J. 1983 May;47(5):596-607. doi: 10.1253/jcj.47.596.
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-PGF1 alpha 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-PGF1 alpha 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-PGF1 alpha 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.
将1.5毫克/千克的花生四烯酸钠（AA）注入16只兔子的冠状动脉。所有兔子均出现心律失常、明显的ST-T段压低和呼吸暂停，7只兔子在注入AA后10分钟内死亡。注射前，血栓素B2（TXB2）值为1.2±0.2纳克/毫升（平均值±标准误），6-酮-前列腺素F1α值为2.1±0.4纳克/毫升。注入AA三分钟后，存活兔子的TXB2值为5.0±1.1，死亡兔子的TXB2值为17.9±6.5纳克/毫升。存活兔子的6-酮-前列腺素F1α值为47.7±4.6，死亡兔子的6-酮-前列腺素F1α值为248.5±69.3纳克/毫升。7只预先用阿司匹林（ASA）治疗的兔子和11只预先用TXA2合成酶特异性抑制剂OKY-046和1581治疗的兔子均未死亡。注入AA后，ASA组和OKY组的TXB2值未发生变化。注入AA后，ASA组的6-酮-前列腺素F1α值未发生变化，OKY组的6-酮-前列腺素F1α值升高。心脏组织学检查结果显示，未预处理组的缺血性改变比ASA组和OKY组更明显。这些结果表明TXA₂在猝死中起作用。前列环素的生成极度增强，提示体内存在抗血栓形成的保护机制。
