Oleic acid lung injury increases plasma prostaglandin levels

Abstract

To determine whether lung injury causes increased plasma prostaglandin (PG) levels, 35 rabbits received oleic acid and 35 served as controls. Half of each group also received 4 ml/kg of Intralipid ® over one hour and at least five in each subgroup received indomethacin 7.5 mg/kg. Arterial and venous plasma concentrations of PGE 2, 6-keto-PGF 1α, and PGF 2α-M were measured. Venous PGE 2 was significantly higher in the oleic acid-injured than in the normal lung group, 1560 ± 270 (Mean ± SEM) versus 880 ± 140 pg/ml (p < .05). Plasma levels were reduced by 50% with indomethacin, but PGE 2 levels remained significantly higher than in the normal lung group, 850 ± 180 versus 480 ± 60 for arterial (p < .05) and 820 ± 140 versus 480 ± 80 for venous (p < .05), respectively. PGF 2α-M levels were significantly higher in the lung injury group, 240 ± 50 versus 50 ± 40 pg/ml for arterial (p < .05) and 220 ± 50 versus 95 ± 40 for venous (p < .05), respectively. These lung injury-related increases in PGE 2 and PGF 2α-M appear related both to increased pulmonary production and to decreased pulmonary clearance. With Intralipid ® infusion, however, arterial PGE 2 increased by 500 ± 260 pg/ml compared to baseline (p < .05) with no change in venous PGE 2, indicating in this instance that the increase in arterial PGE 2 levels is related to increased pulmonary production.