Optimal timing and temperature for hyperthermic preconditioning in an animal model of fecal peritonitis.
The impact of immune parameters in the mechanism of hyperthermia is yet to be explained. In this study, the optimal timing and temperature of thermal treatment for reversing the abnormal immunologic parameters obtained in a rat model of peritonitis were planned to be determined. Male Sprague-Dawley rats were grouped as sham, control peritonitis, and thermally treated rats at the time of peritonitis or 4 h prior to induction of peritonitis both at 40 and 42 degrees C. Peritonitis was induced by the cecal ligation and perforation model. Eight hours after the induction of peritonitis, rats were sacrified and samples were taken for measurements of CD4+, CD8+, CD(11b), B cells, NK cells, and tumor necrosis factor alpha (TNFalpha) and thiobarbituric acid-reactive substances (TBARS) levels. CD4+ expression and B cell amount were decreased whereas TNFalpha levels, CD8+ and CD(11b) expression, and NK cell amount were found to be increased in the control peritonitis group when compared to the sham group. Peritonitis induction also increased TBARS levels in liver tissue. Hyperthermic preconditioning at either 40 or 42 degrees C applied 4 h prior to peritonitis induction returned all parameters to their normal levels, which is similar to the results of the sham laparotomy group. The results of TNFalpha values in preconditioned rats were varied according to the temperature that was applied. The levels were increased at 40 degrees C, whereas they showed a decline at 42 degrees C. Hyperthermic preconditioning prevented the oxidative damage in liver as well as TNFalpha elevation, particularly at 42 degrees C. Results from this study suggest that hyperthermic preconditioning 4 h prior to the onset of septic events may improve the adverse outcome in sepsis.
Güllüoğlu
Bahadir M
BM
Department of General Surgery, Marmara University School of Medicine, Istanbul, Turkey.
Aksoy
B Serdar
BS
Ozveri
Emel Sayin
ES
Yüksel
Meral
M
Demiralp
Emel E
EE
Aktan
A Ozdemir
AO
D000704:Analysis of Variance; D000818:Animals; D000954:Antigens, Surface / Q000032:analysis; D001402:B-Lymphocytes / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D039481:CD11b Antigen / Q000032:analysis; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D004195:Disease Models, Animal; D005243:Feces / Q000382:microbiology*; D006979:Hyperthermia, Induced; D016130:Immunophenotyping; D019194:Ischemic Preconditioning / Q000379:methods*; D007694:Killer Cells, Natural / Q000276:immunology; D008099:Liver / Q000378:metabolism; D018655:Lymphocyte Count; D008297:Male; D010538:Peritonitis / Q000276:immunology / Q000628:therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013696:Temperature; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000954:Antigens, Surface; D015415:Biomarkers; D039481:CD11b Antigen; D015704:CD4 Antigens; D016827:CD8 Antigens; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha