title: Persistent and progressive pulmonary fibrotic changes in a model of fat embolism.
abstract: BACKGROUND
  Fat embolism (FE) after trauma and some orthopedic procedures is known to cause acute lung injury, including acute respiratory distress syndrome. However, its potential long-term effects on the lung are unknown. A previous study using a rat model of FE found significant histopathologic changes in the lungs after intravenous injection of triolein for up to 11 days. This study detailed the persistence of the lung damage and investigated the input of the renin-angiotensin system in its pathology.
  
  
  METHODS
  Unanesthetized rats were injected via the tail vein with 0.2 mL saline or triolein. After euthanasia, at 3 weeks or 6 weeks, lung sections were stained to highlight cellular structure, presence of collagen and fat, or immunolabeled for smooth muscle actin or angiotensin peptides.
  
  
  RESULTS
  At 3 weeks or 6 weeks after triolein injection, there was no dilatation of the heart or inferior vena cava, no congestion of the liver or spleen, no adventitial edema, nor was fluid present in alveoli or pleural cavity as reported in animals at earlier time points. Persisting pathology included reduced lumen patency, thickening of the media of small arteries and arterioles, and vascular and septal inflammation. Although the fat content of the lung decreased from week 3 to week 6, there was a progressive increase in collagen, smooth muscle actin, and angiotensin peptides.
  
  
  CONCLUSIONS
  This model extends the effect of FE on pulmonary pathology to 6 weeks, revealing persistent vasculitis, septal inflammation, and progressive fibrotic changes which are associated with increased presence of angiotensin peptides.
authors.affiliation: Department of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, MO 64108-2792, USA.
authors.forename: Alan M
authors.initials: AM
authors.lastname: Poisner
authors.forename: Federico
authors.initials: F
authors.lastname: Adler
authors.forename: Bruce
authors.initials: B
authors.lastname: Uhal
authors.forename: Terence E
authors.initials: TE
authors.lastname: McIff
authors.forename: John P
authors.initials: JP
authors.lastname: Schroeppel
authors.forename: Aaron
authors.initials: A
authors.lastname: Mehrer
authors.forename: Betty L
authors.initials: BL
authors.lastname: Herndon
authors.forename: Kamani M
authors.initials: KM
authors.lastname: Lankachandra
authors.forename: Agostino
authors.initials: A
authors.lastname: Molteni
mesh_terms: D000809:Angiotensins / Q000378:metabolism; D000818:Animals; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D004620:Embolism, Fat / Q000150:complications*; D005223:Fats / Q000032:analysis; D008168:Lung / Q000737:chemistry / Q000473:pathology; D008297:Male; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000809:Angiotensins; D005223:Fats; D003094:Collagen