Salzman P M, Salmon J A, Moncada S
J Pharmacol Exp Ther. 1980 Oct;215(1):240-7.
Superfused spiral strips of rabbit intrapulmonary artery (i.p.a.) were contracted by arachidonic acid (AA) and by the following substances in order of potency: prostaglandin (PG) endoperoxide analog (U46619) > PGH2 > PGF2 alpha. Intrapulmonary artery strips were consistently relaxed by PGE2 and by the enzyme inhibitors, indomethacin, aspirin, meclofenamic acid and 1-pentylimidazole. These latter inhibitors of cyclooxygenase and thromboxane (TX) synthetase also blocked the AA-induced contraction of rabbit i.p.a. Prostacyclin had no effect on the i.p.a. or produced either a small contraction or relaxation. TXA2, formed by incubating horse platelet microsomes with PHG2, always contracted the tissue and was more potent than the parent endoperoxide. Incubations of [14C]AA with i.p.a. produced mainly [14C]-6-keto-PGF1 alpha (he breakdonw product of prostacyclin ) and [14C]TXB2 (the breakdown product of TXA2); the identities of these products were confirmed by radioimmunoassay and by gas chromatography-mass spectrometry. The synthesis of TXB2 by i.p.a. cannot be attributed to adhering lung tissue or platelets and appears to be produced by the vascular tissue itself. It is concluded that, although both prostacyclin and thromboxane may contribute to the resting tone of the rabbit i.p.a., the response to AA is mainly due to production of TXA2.
兔肺动脉（i.p.a.）的灌注螺旋条被花生四烯酸（AA）以及以下物质按效力顺序收缩：前列腺素（PG）内过氧化物类似物（U46619）> PGH2 > PGF2α。肺动脉条持续被PGE2以及酶抑制剂吲哚美辛、阿司匹林、甲氯芬那酸和1-戊基咪唑松弛。这些环氧化酶和血栓素（TX）合成酶的抑制剂也阻断了AA诱导的兔i.p.a.收缩。前列环素对i.p.a.无影响或产生轻微收缩或松弛。通过将马血小板微粒体与PHG2孵育形成的TXA2总是使组织收缩，且比母体内过氧化物更有效。[14C]AA与i.p.a.孵育主要产生[14C]-6-酮-PGF1α（前列环素的分解产物）和[14C]TXB2（TXA2的分解产物）；这些产物的身份通过放射免疫测定和气相色谱-质谱法得到证实。i.p.a.合成TXB2不能归因于附着的肺组织或血小板，似乎是由血管组织自身产生的。结论是，虽然前列环素和血栓素都可能对兔i.p.a.的静息张力有贡献，但对AA的反应主要是由于TXA2的产生。
