PMID- 8838134
OWN - NLM
STAT- MEDLINE
DCOM- 19961216
LR  - 20191024
IS  - 0190-2148 (Print)
IS  - 0190-2148 (Linking)
VI  - 22
IP  - 1
DP  - 1996 Jan-Feb
TI  - Sequential appearance of inflammatory mediators in rat bronchoalveolar lavage 
      fluid after oleic acid-induced lung injury.
PG  - 33-49
AB  - The oleic acid (OA) model of rat lung injury was originally developed as a model 
      of fat embolism syndrome. A single intravenous dose of pure OA causes an acute 
      diffuse lung injury, which, in its initial stages, histologically and 
      physiologically resembles human ARDS. Rat lungs acutely injured by intravenous OA 
      manifest increased levels of ICAM-1 within 30-60 min. This study shows that human 
      umbilical vein endothelial cells (HUVEC) can be used in a bioassay to reveal some 
      of the adhesion molecule stimulating activities present in bronchoalveolar lavage 
      fluid (BALF) from post-OA-injected rats: (1) There is an as yet unidentified 
      ICAM-1 and ELAM (E Selectin) inducing activity in BALF within 15 min of OA 
      injection that is not TNF alpha; there is very little measurable tumor necrosis 
      factor-alpha (TNF alpha) in 15 min BALF (BALF15). (2) BALF15 also stimulates 
      cultured macrophage derived from BALF of normal rat lungs to produce TNF alpha. 
      (3) By 60 min after OA injection, 50-75% of the ICAM-1 and ELAM inducing activity 
      in BALF (BALF60) is TNF alpha; BALF60 contains about 250-280 pg/mL TNF alpha. The 
      other 25-50% adhesion molecule-inducing activity in BALF60 is unidentified. (4) 
      The ICAM-1-inducing activity of pure TNF alpha was equal to that of BALF60 
      containing equivalent concentrations of TNF alpha. The ELAM inducing activity of 
      pure TNF alpha, however, was about 1/2 that of BALF60 containing equivalent 
      concentrations of TNF alpha. The time courses for ICAM and ELAM stimulation with 
      pure TNF alpha or BALF60 containing equivalent levels of TNF alpha were the same. 
      The identity of the mediators in BALF15 and BALF60 that are not TNF alpha and the 
      mechanisms by which OA injection stimulates cytokine production remain to be 
      elucidated.
FAU - Syrbu, S
AU  - Syrbu S
AD  - Department of Pharmacology, University of Connecticut Health Center, Farmington, 
      USA.
FAU - Thrall, R S
AU  - Thrall RS
FAU - Smilowitz, H M
AU  - Smilowitz HM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Exp Lung Res
JT  - Experimental lung research
JID - 8004944
RN  - 0 (E-Selectin)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 2UMI9U37CP (Oleic Acid)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/*chemistry
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - E-Selectin/biosynthesis
MH  - Inflammation Mediators/*analysis
MH  - Injections, Intravenous
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Lung Diseases/*chemically induced/metabolism
MH  - Macrophages, Alveolar/drug effects/metabolism
MH  - Male
MH  - Models, Biological
MH  - Oleic Acid
MH  - Rats
MH  - Rats, Inbred F344
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/analysis/immunology
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.3109/01902149609074016 [doi]
PST - ppublish
SO  - Exp Lung Res. 1996 Jan-Feb;22(1):33-49. doi: 10.3109/01902149609074016.