[The study of thromboxane A2 and prostacyclin in oleic acid-induced lung injury in dogs].
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.
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D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood*; D000818:Animals; D004285:Dogs; D005260:Female; D008297:Male; D009829:Oleic Acids; D012128:Respiratory Distress Syndrome / Q000097:blood* / Q000139:chemically induced; D013928:Thromboxane A2 / Q000097:blood*
D009829:Oleic Acids; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha