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细胞在各种侵扰下可由膜磷脂释放出20碳花生四烯酸,其氧化代谢产物包括前列腺素(PGs)、前列环素(PGI_2)、血栓烷(TXs)以及白三烯(LTs)参与肺血管、支气管的舒缩活动,白细胞、血小板聚集等生理过程,并影响肺毛细血管的通透性。从而参与ARDS 的病理生理过程。花生四烯酸可进入环氧合酶通路而形成环内过氧化物,后者在前列环素合成酶或血栓烷合成酶的作用下分别转化为前列环素与血栓烷A_2(TXA_2)。在前列腺素合成酶系中,环氧合酶可被阿斯匹林、消炎痛或Ibuprofen 所抑制;而血栓烷合成酶可为咪唑或咪唑衍生物OKY-O46所阻断。花生四烯酸
Cells can release 20-arachidonic acid from membrane phospholipids under various perturbations, and their oxidative metabolites include prostaglandins (PGs), prostacyclin (PGI_2), thromboxanes (TXs), and leukotrienes (LTs) Blood vessels, bronchial contraction and contraction activities, leukocytes, platelet aggregation and other physiological processes, and affect the permeability of pulmonary capillaries. Thus participating in the pathophysiology of ARDS. Arachidonic acid can enter the cyclooxygenase pathway and form an intraperoxide, which is converted to prostacyclin and thromboxane A 2 (TXA 2) by prostacyclin synthase or thromboxane synthase, respectively. In the prostaglandin synthase system, cyclooxygenase can be inhibited by aspirin, indomethacin or Ibuprofen; and thromboxane synthase can be blocked by the imidazole or imidazole derivative OKY-O46. Arachidonic acid