de Kergommeaux B D, Ali M, McDonald J W
Prostaglandins Leukot Med. 1983 Jun;11(2):225-31. doi: 10.1016/0262-1746(83)90022-7.
Rabbit aorta and pulmonary artery were incubated in the presence and absence of added arachidonic acid, and the synthesis of prostaglandin I2 (PGI2) and thromboxane A2 (TXA2) was studied by radioimmunoassay of the stable hydrolysis products 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2). Aorta and pulmonary artery synthesized 6-keto-PGF1 alpha and TXB2 in ratios of 10-60:1. The pulmonary artery appeared to synthesize relatively more thromboxane. This may be because of a thinner muscular layer, since smooth muscle cells have previously been shown to produce only 6-keto-PGF1 alpha, while endothelial cells synthesize both compounds. Pretreatment of animals with aspirin (ASA) in a dose of 1 mg/kg strongly inhibited synthesis of both products by aorta and pulmonary artery. A dose of 0.1 mg/kg was without effect. After a single intravenous dose of ASA, the inhibitory effect was maximal between 4 and 12 hours and was still marked at 24 hours, increasing to normal at approximately 48 hours. Selective suppression of platelet cyclooxygenase activity with sparing of the vascular enzyme appears to be difficult to achieve.
将兔主动脉和肺动脉分别在添加和未添加花生四烯酸的情况下进行孵育，并通过对稳定水解产物6-酮-前列腺素F1α（6-酮-PGF1α）和血栓素B2（TXB2）进行放射免疫测定来研究前列腺素I2（PGI2）和血栓素A2（TXA2）的合成。主动脉和肺动脉合成6-酮-PGF1α和TXB2的比例为10 - 60:1。肺动脉似乎合成相对更多的血栓素。这可能是因为其肌层较薄，因为先前已表明平滑肌细胞仅产生6-酮-PGF1α，而内皮细胞可合成这两种化合物。以1mg/kg的剂量用阿司匹林（ASA）预处理动物可强烈抑制主动脉和肺动脉中这两种产物的合成。0.1mg/kg的剂量则无作用。单次静脉注射ASA后，抑制作用在4至12小时之间最大，在24小时时仍很明显，大约在48小时时恢复正常。似乎难以实现选择性抑制血小板环氧化酶活性而不影响血管酶活性。
