title: Human blood vessels release tumor necrosis factor-alpha from a smooth muscle cell source.
abstract: OBJECTIVE
  In septic shock, the principal source of increased plasma concentrations of tumor necrosis factor alpha (TNF) is considered to be the macrophage. Release from the macrophage is stimulated by bacterial lipopolysaccharide (endotoxin). We tested the hypothesis that vascular tissue also responds to endotoxin by releasing TNF.
  
  
  METHODS
  Prospective repeated measures analysis of timed-release curves.
  
  
  METHODS
  Anesthesia research laboratory in an academic medical center.
  
  
  METHODS
  With Institutional Review Board approval and patient consent, segments of internal mammary artery and saphenous vein were obtained during coronary artery bypass surgery.
  
  
  METHODS
  None
  
  
  RESULTS
  Segments of saphenous veins were incubated for 24 hrs in the presence or absence of bacterial lipopolysaccharide. At 0.5, 1, 3, 6, and 24 hrs, medium was assayed for TNF. In other experiments, smooth muscle cells were cultured from saphenous veins, incubated with our without bacterial lipopolysaccharide, and a time-course of TNF release determined. Bacterial lipopolysaccharide (20 micrograms/mL) significantly stimulated release of TNF from venous tissue in a time-dependent manner. At 0.5 hrs, TNF was undetectable in untreated tissue and was 48 +/- 8 U/g wet tissue weight in the presence of bacterial lipopolysaccharide. At 3 hrs, TNF was 43 +/- 27 U/g wet tissue weight in untreated and 388 +/- 185 U/g wet tissue weight in treated (p < .01 vs. control) tissue. Segments of internal mammary artery responded in a similar manner. In smooth muscle cells cultured from saphenous vein and internal mammary artery, bacterial lipopolysaccharide triggered the release of TNF. At 3 hrs, the release of TNF in control cells was 0.2 +/- 0.15 U/mg cell protein and 17 +/- 2 U/mg in the presence of 20 micrograms/mL of bacterial lipopolysaccharide (p < .01 vs. control).
  
  
  CONCLUSIONS
  Human blood vessels, both artery and vein, produce TNF potentially from a smooth muscle cell source in response to bacterial lipopolysaccharide.
authors.affiliation: Division of Basic Medical Science, Mercer University School of Medicine, Macon, GA., USA.
authors.forename: W H
authors.initials: WH
authors.lastname: Newman
authors.forename: L M
authors.initials: LM
authors.lastname: Zhang
authors.forename: S K
authors.initials: SK
authors.lastname: Leeper-Woodford
authors.forename: M R
authors.initials: MR
authors.lastname: Castresana
mesh_terms: D000704:Analysis of Variance; D002478:Cells, Cultured; D004926:Escherichia coli; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism; D008323:Mammary Arteries; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D012501:Saphenous Vein; D012772:Shock, Septic / Q000097:blood / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha