Oleic acid lung injury increases plasma prostaglandin levels

J. R. Hageman*, K. McCulloch, C. E. Hunt, M. Cobb, B. Quade, F. Crussi, Lauren M Pachman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

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 PGE2, 6-keto-PGF, and PGF-M were measured. Venous PGE2 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 PGE2 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-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 PGE2 and PGF-M appear related both to increased pulmonary production and to decreased pulmonary clearance. With Intralipid® infusion, however, arterial PGE2 increased by 500 ± 260 pg/ml compared to baseline (p < .05) with no change in venous PGE2, indicating in this instance that the increase in arterial PGE2 levels is related to increased pulmonary production.

Original languageEnglish (US)
Pages (from-to)157-164
Number of pages8
JournalProstaglandins, Leukotrienes and Essential Fatty Acids
Volume35
Issue number3
DOIs
StatePublished - Jan 1 1989

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology

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