Cui S H
Zhonghua Jie He He Hu Xi Za Zhi. 1989 Feb;12(1):24-6, 61.
Acute lung injury was produced by intravenous injection of oleic acid. After oleic acid injection, PaO2 was decreased, dogs were involved in respiratory distress. Histological examination indicated aggregation of leukocytes in microvasculature, interstitial and intraalveolar pulmonary edema and congestion in the lung. Using radioimmunoassay technique, changes in arterial and venous plasma levels of stable metabolite of thromboxane A2 (TXA2), thromboxane B2 (TXB2) have been observed. After oleic acid administration, plasma 6-keto-PGF1alpha level was markedly elevated with two peaks. 6-keto-PGF1alpha level in arteries was higher in concentration than in veins. It was suggested that the lung might synthesis a great quantity of prostacyclin entering the systemic circulation. TXB2 was markedly elevated in plasma, which was more in veins than in arteries. A significant arteriovenous difference suggests that there might be extrapulmonary sources contributing to the elevation of plasma TXB2 in oleic acid induced lung injury in dogs. After treatment with large dose of anisodamine (654-2), platelets and leukocytes aggregation could be inhibited as well as the synthesis of TXA2 and prostacyclin. 654-2 might play a role of cyclo-oxygenase inhibitor. It was suggested that 654-2 reduce synthesis of the precursors of TXA2 and prostacyclin, reduce pulmonary edema and might be a therapeutical effect to lung injury.
通过静脉注射油酸来诱导急性肺损伤。注射油酸后，动脉血氧分压（PaO2）降低，犬出现呼吸窘迫。组织学检查显示肺微血管内白细胞聚集、间质和肺泡内肺水肿以及肺充血。采用放射免疫测定技术，观察到血栓素A2（TXA2）的稳定代谢产物血栓素B2（TXB2）在动脉和静脉血浆中的水平变化。给予油酸后，血浆6-酮-前列腺素F1α（6-keto-PGF1α）水平显著升高并出现两个峰值。动脉中6-keto-PGF1α的浓度高于静脉。提示肺可能合成大量前列环素进入体循环。血浆中TXB2显著升高，静脉中的含量高于动脉。显著的动静脉差异表明，在油酸诱导的犬肺损伤中，可能存在肺外来源导致血浆TXB2升高。用大剂量山莨菪碱（654-2）治疗后，血小板和白细胞聚集以及TXA2和前列环素的合成均可被抑制。654-2可能起到环氧化酶抑制剂的作用。提示654-2可减少TXA2和前列环素前体的合成，减轻肺水肿，对肺损伤可能具有治疗作用。
