title: Acute portal hypertension increases ileal vulnerability to platelet-activating factor in rats.
abstract: BACKGROUND
  Patients with portal hypertension can easily develop sepsis of enteric origin after suffering severe trauma and hemorrhagic shock. Platelet-activating factor (PAF) is one of the key mediators of such stress. The aim of this study was to investigate whether portal hypertension increases the vulnerability of the ileum to PAF.
  
  
  METHODS
  Seven days after surgery, PAF (1.5 microg/kg) was intravenously injected into portal stenosis (PS) rats and sham-operated rats. The levels of tumor necrosis factor-alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (CINC), and endotoxin in portal plasma were determined. The levels of PAF receptor (PAFR), TNF-alpha, and CINC mRNA in the ileum were also investigated.
  
  
  RESULTS
  After PAF administration, PS rats showed (1) significantly higher portal plasma levels of TNF-alpha, CINC, and endotoxin; (2) higher histological damage scores in the ileum; (3) more infiltrating neutrophils in the ileum; and (4) a significantly higher mortality rate than sham-operated rats (P < 0.01). However, PAFR mRNA levels were similar in the two groups. The CINC mRNA level in the ileum of PS rats was increased from 1 to 4 h after PAF administration, while that of the sham-operated rats was transiently increased at 1 h.
  
  
  CONCLUSIONS
  Portal hypertension increases the vulnerability of the ileum to PAF. These findings suggest that conditions which causes PAF production may be dangerous in patients with portal hypertension.
authors.affiliation: Department of Surgery II, Hamamatsu University School of Medicine, Hamamatsu, Japan. tasaka@hama-med.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Sakaguchi
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Oda
authors.forename: A
authors.initials: A
authors.lastname: Ichiyama
authors.forename: S
authors.initials: S
authors.lastname: Baba
mesh_terms: D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000097:blood / Q000235:genetics; D006133:Growth Substances / Q000097:blood / Q000235:genetics; D006975:Hypertension, Portal / Q000503:physiopathology*; D007082:Ileum / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology*; D036341:Intercellular Signaling Peptides and Proteins; D007700:Kinetics; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D009504:Neutrophils / Q000502:physiology; D010972:Platelet Activating Factor / Q000494:pharmacology*; D010980:Platelet Membrane Glycoproteins / Q000235:genetics; D011169:Portal Vein / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics
chemical_list: D019743:Chemokines, CXC; D002630:Chemotactic Factors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D014409:Tumor Necrosis Factor-alpha; C039351:platelet activating factor receptor