Washing with sample solvent eluted the fatty ..... pressure observed early in these lung injury models. PGE2 is considered .... JR, McCulloch. K. Gora P. Olsen E.
ProstaglandinsLeukotrienesand Medicine 25: 105-122,1986
THE EARLY INVOLVEMENT OF PULMONARY IN HYPEROXIC
PROSTAQLAMINB
LUNG INJURY
Joseph R. Hagernan. M.D., Scott Babler. Stephen C. Lee. Michael Cobb, Lauren M. Pachman. Lewis J. Smith, Carl E. Hunt [reprint requests JRHI Evanston Hospital: Dept. of Pediatrics: 2850 Ridge Avenue; Evenston. IL.. 60201. USA. Presented in part at Anaheim, California
the American
Thoracic
Society
meeting.
May
1885:
ABSTRACT To further study the role of arechidonic acid metabolites in the development of hyperoxic lung injury and the function of PMNs and/or elveolar macrophages in facilitating this role. we exposed adult rabbits to >Q5% 02 or air for 24, 40. 40. or 65 hours. At the end of each study. bronchoalveolar lavage [BALI of the left lung was performed, and the right lung was inflated and fixed for light and electron microscopy. PC3E2. 6-keto-PElFTo and thromboxene 62 were measured by RIA in arterial and venous plasma at the beginning and end of each study and in BAL fluid obtained et sacrifice. Production of these three PQs by BAL cells placed in cell culture was also measured. Significant hyperoxic lung injury did not develop until 65 hours. as evidenced by significant increase in BAL total protein and percent PMNs. and by morphologic findings. At 40 hours, however, BAL fluid PGE2 and B-keto-PQFlo increased and BAL cell production of all 3 P(3s was significantly increased [p
