Endo S, Akiyama K
Clinical Research Center for Allergy and Rheumatology, National Sagamihara Hospital.
Nihon Rinsho. 1996 Nov;54(11):3045-8.
Lung tissues produce a large amount of Thromboxane (Tx) A2. In addition to platelet aggregation and artery smooth muscle contraction, TxA2 strongly induces airway smooth muscle contraction and bronchial hyperresponsiveness. Not only TxA2, but many arachidonate cyclooxygenase metabolites such as PGD2, PGF2 alpha, PGH2, and others stimulate TP (PGH2/TxA2) receptor and can take a pathophysiological role for bronchial asthma. Several compounds competitively antagonizing TP receptor have been developed and being proved to have beneficial effects for treating of bronchial asthma in clinical. In this review the efficacy and usage of TP receptor antagonists for bronchial asthma was discussed.
肺组织会产生大量血栓素(Tx)A2。除了导致血小板聚集和动脉平滑肌收缩外,TxA2还会强烈诱导气道平滑肌收缩和支气管高反应性。不仅TxA2,许多花生四烯酸环氧化酶代谢产物,如前列腺素D2、前列腺素F2α、前列腺素H2等,都会刺激TP(前列腺素H2/血栓素A2)受体,并可能在支气管哮喘的病理生理过程中发挥作用。已经研发出几种竞争性拮抗TP受体的化合物,并且在临床上已证明它们对治疗支气管哮喘有有益作用。在这篇综述中,讨论了TP受体拮抗剂治疗支气管哮喘的疗效和用法。