Ogletree M L
Fed Proc. 1987 Jan;46(1):133-8.
Thromboxane (Tx) A2 is a biologically potent and chemically unstable metabolite of prostaglandin endoperoxides. Recent developments in measurement techniques and the availability of both selective inhibitors of Tx synthetase and TxA2 receptor antagonists have facilitated the implication of TxA2 as a physiological modulator and as a mediator in thrombotic, vasospastic, and bronchospastic conditions. TxA2 is synthesized by platelets and contributes to platelet activation and irreversible platelet aggregation in physiological hemostasis and in thrombosis (e.g., unstable angina, stroke). TxA2 is also synthesized in intestinal, pulmonary, and renal tissues by cells other than platelets. Particularly in these tissues, TxA2 appears to act as a physiological modulator of changes in blood flow distribution and airway caliber. Strong stimuli for TxA2 release from these tissues may initiate ulcer, pulmonary hypertension, bronchoconstriction, and renal vasoconstriction. Evidence supports participation of TxA2 and/or TxA2 receptors in modulation of natural cytotoxic cell cytotoxicity, in tumor growth and metastasis, in complications of pregnancy (e.g., preeclampsia), and in the progression of ischemic injury after coronary artery occlusion. This evidence supports pivotal involvement of TxA2 in pathophysiology and provides a strong rationale for pursuing TxA2-blocking strategies in drug development.
血栓素（Tx）A2是前列腺素内过氧化物的一种生物活性强且化学性质不稳定的代谢产物。测量技术的最新进展以及Tx合成酶选择性抑制剂和TxA2受体拮抗剂的可得性，促进了TxA2作为生理调节剂以及在血栓形成、血管痉挛和支气管痉挛病症中作为介质的作用的研究。TxA2由血小板合成，在生理止血和血栓形成（如不稳定型心绞痛、中风）中促进血小板活化和不可逆的血小板聚集。TxA2也由血小板以外的细胞在肠道、肺和肾组织中合成。特别是在这些组织中，TxA2似乎作为血流分布和气道管径变化的生理调节剂。来自这些组织的TxA2释放的强烈刺激可能引发溃疡、肺动脉高压、支气管收缩和肾血管收缩。有证据支持TxA2和/或TxA2受体参与自然杀伤细胞细胞毒性的调节、肿瘤生长和转移、妊娠并发症（如先兆子痫）以及冠状动脉闭塞后缺血性损伤的进展。这一证据支持TxA2在病理生理学中的关键作用，并为在药物开发中采用TxA2阻断策略提供了有力的理论依据。
