title: Pentoxyphilline as a cyclooxygenase (cox-2) inhibitor in experimental sepsis.
abstract: BACKGROUND
  The aim of this study is to assess the impact of pentoxyphilline (PTX) on the pattern of serum concentrations of certain pro-inflammatory cytokines and their soluble receptors in relation to the animal's survival period.
  
  
  METHODS
  Diffuse peritonitis was elicited by means of cecal ligation and puncture (CLP) in 45 adult Wistar rats. The pattern of soluble TNF receptor p55 type 1 and p75 type 2 in reference to TNF-alpha and IL-1beta concentration in animals with experimental diffuse peritonitis (EDP) was estimated. All animals were divided into 3 groups.
  
  
  RESULTS
  In both groups where animals received medication, the percentage of survival was higher than in the controls. An increase in CRP concentration was observed in all study animals. An increase in TNFalpha concentration was noted during the first 12 hours of the experiment. There was an increase in soluble TNFR p55 concentrations in all study groups until the 24th hour of the experiment, then a decrease until the end of the observation period. The concentration of soluble TNF p75 receptor gradually increased over time in all groups. In group I a constant rise of IL-1beta serum concentration was observed.
  
  
  CONCLUSIONS
  Pentoxyphilline administration in animals in the early stage of diffuse peritonitis causes the TNFalpha serum concentration to decrease, but it does not improve the overall survival period. Late pentoxyphilline administration does not alter the course of diffuse peritonitis in rat.
authors.affiliation: Department of General Surgery, Medical University of Łódź, Łódź, Poland. bogdanm@ventura.pl
authors.forename: Bogdan
authors.initials: B
authors.lastname: Modzelewski
authors.forename: Adam
authors.initials: A
authors.lastname: Janiak
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000097:blood; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D004195:Disease Models, Animal; D007274:Injections, Intraperitoneal; D007375:Interleukin-1 / Q000097:blood; D007527:Isoenzymes / Q000037:antagonists & inhibitors*; D008297:Male; D010431:Pentoxifylline / Q000494:pharmacology*; D010538:Peritonitis / Q000150:complications / Q000201:enzymology / Q000209:etiology / Q000276:immunology; D011451:Prostaglandin-Endoperoxide Synthases; D051381:Rats; D017208:Rats, Wistar; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I; D018805:Sepsis / Q000188:drug therapy* / Q000201:enzymology / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015703:Antigens, CD; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007375:Interleukin-1; D007527:Isoenzymes; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D010431:Pentoxifylline