Neri Serneri G G, Abbate R, Panetta A, Pinto S, Favilla S, Prisco D, Gensini G F
Thromb Res. 1987 Apr 15;46(2):303-16. doi: 10.1016/0049-3848(87)90292-1.
Thromboxane A2 (TxA2) generation and 1-14C arachidonic acid (AA) metabolism by platelets (stimulated with thrombin) were studied in vitro in 16 patients with unstable angina both during the acute and chronic inactive phase of the angina. Eight patients with stable effort angina and 21 controls were also investigated. In acute unstable angina 1-14C AA metabolism was significantly increased through cyclooxygenase pathway resulting in a higher selective TxA2 generation than in stable effort angina and in controls (p less than 0.01). No differences were found between patients with stable effort angina and controls. The alterations in AA metabolism were no longer found when patients reverted to the inactive phase of angina. TxA2 generation by platelets was independent of the number of the daily ischemic attacks (r = 0.17, ns) in patients with unstable angina. Present results indicate that an altered intraplatelet AA metabolism leading to the increased TxA2 synthesis occurs simultaneously with the conversion of angina from the chronic to the acute phase.
在16例不稳定型心绞痛患者心绞痛的急性期和慢性静止期，均于体外研究了（用凝血酶刺激的）血小板生成血栓素A2（TxA2）及1-14C花生四烯酸（AA）代谢情况。还对8例稳定型劳力性心绞痛患者和21名对照者进行了研究。在急性不稳定型心绞痛中，通过环氧化酶途径的1-14C AA代谢显著增加，导致TxA2生成选择性高于稳定型劳力性心绞痛患者和对照者（p<0.01）。稳定型劳力性心绞痛患者与对照者之间未发现差异。当患者恢复到心绞痛静止期时，未再发现AA代谢改变。不稳定型心绞痛患者血小板生成TxA2与每日缺血发作次数无关（r=0.17，无统计学意义）。目前结果表明，导致TxA2合成增加的血小板内AA代谢改变与心绞痛从慢性期转变为急性期同时发生。
