title: The effect of hyperthermic preconditioning on the immune system in rat peritonitis.
abstract: OBJECTIVE
  To assess whether hyperthermic (HT) preconditioning prevents the lethal effects of peritonitis by acting on the immune system.
  
  
  METHODS
  Prospective, controlled, experimental study.
  
  
  METHODS
  Laboratory and animal facility of the university.
  
  
  METHODS
  Adult male Sprague-Dawley rats.
  
  
  METHODS
  In the HT groups animals were subjected to hyperthermia (42 degrees C, 15 min) and 8 h later peritonitis (P) (n = 14) was induced. In the normothermic (NT) groups, animals were subjected to normothermia (38 degrees C, 15 min) and 8 h later peritonitis (n = 14) was induced. Each group had a corresponding sham laparotomy group (n = 14). Six rats from each group were allowed to live 7 days for survival. In the control group (n = 4), rats were not anesthetized or heat treated.
  
  
  RESULTS
  Sixteen hours after peritonitis and laparotomy, rats were killed. Blood was taken to measure the percentage of CD(4)(+), CD(8)(+), CD(4)(+)CD(56)(+), CD(8)(+) CD(11 b)(+), NK(+), B cells and the level of tumor necrosis factor. Grading of peritonitis and the measurement of free oxygen radicals in the peritoneal fluid were undertaken. All rats in the HT + P and sham laparotomy groups survived for 7 days, while in the NT + P group two rats died in 7 days. HT decreased the severity of peritonitis and increased the free oxygen radicals in the peritoneal fluid; however, the difference did not reach statistical significance. HT prevented the decrease in CD(4)(+) and B cells and the increase in CD(11 b)(+).
  
  
  CONCLUSIONS
  HT may have a protective role in sepsis by reducing the severity of peritonitis. A causal relation between hyperthermia and an improved immune system seems possible.
authors.affiliation: Marmara University School of Medicine, Departments of General Surgery, Altunizade 81190, Istanbul, Turkey.
authors.forename: E S
authors.initials: ES
authors.lastname: Ozveri
authors.forename: A
authors.initials: A
authors.lastname: Bekraki
authors.forename: A
authors.initials: A
authors.lastname: Cingi
authors.forename: M
authors.initials: M
authors.lastname: Yuksel
authors.forename: E E
authors.initials: EE
authors.lastname: Demiralp
authors.forename: B C
authors.initials: BC
authors.lastname: Yegen
authors.forename: A O
authors.initials: AO
authors.lastname: Aktan
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000737:chemistry; D001402:B-Lymphocytes / Q000378:metabolism; D015704:CD4 Antigens / Q000097:blood; D019002:CD56 Antigen / Q000097:blood; D016827:CD8 Antigens / Q000097:blood; D004195:Disease Models, Animal; D005609:Free Radicals / Q000032:analysis; D006979:Hyperthermia, Induced / Q000379:methods*; D016130:Immunophenotyping; D019194:Ischemic Preconditioning / Q000379:methods*; D007694:Killer Cells, Natural / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000097:blood; D008297:Male; D010538:Peritonitis / Q000097:blood / Q000276:immunology* / Q000517:prevention & control*; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015704:CD4 Antigens; D019002:CD56 Antigen; D016827:CD8 Antigens; D005609:Free Radicals; D016177:Macrophage-1 Antigen; D014409:Tumor Necrosis Factor-alpha