title: Body temperature control in sepsis-induced acute lung injury.
abstract: Body temperature is precisely regulated to maintain homeostasis in homeothermic animals. Although it remains unproved whether change of body temperature constitutes a beneficial or a detrimental component of the septic response, temperature control should be an important entity in septic experiments. We investigated the effect of body temperature control on the lipopolysaccharide (LPS)-induced lung injury. Acute lung injury in rats was induced by intratracheal spray of LPS and body temperature was either clamped at 37 degrees C for 5 hours or not controlled. The severity of lung injury was evaluated at the end of the experiment. Intratracheal administration of aerosolized LPS caused a persistent decline in body temperature and a significant lung injury as indicated by an elevation of protein-concentration and LDH activity in the bronchoalveolar lavage (BAL) fluid and wet/dry weight (W/D) ratio of lungs. Administration of LPS also caused neutrophil sequestration and lipid peroxidation in the lung tissue as indicated by increase in myeloperoxidase (MPO) activity and malondialdehyde (MDA) production, respectively. Control of body temperature at 37 degrees C after LPS (LPS/BT37, n = 11) significantly reduced acute lung injury as evidenced by decreases in BAL fluid protein concentration (983 +/- 189 vs. 1403 +/- 155 mg/L) and LDH activity (56 +/- 10 vs. 123 +/- 17 deltamAbs/min) compared with the LPS group (n = 11). Although the W/D ratio of lung and MDA level were lower in the rats received temperature control compared with those received LPS only, the differences were not statistically significant. Our results demonstrated that intratracheal administration of aerosolized LPS induced a hypothermic response and acute lung injury in rats and controlling body temperature at a normal range may alleviate the LPS-induced lung injury.
authors.affiliation: Division of Clinical Pathology, Department of Pathology, Tri-Service General Hospital, Taipei, Taiwan, ROC.
authors.forename: Giueng-Chueng
authors.initials: GC
authors.lastname: Wang
authors.forename: Wei-Ming
authors.initials: WM
authors.lastname: Chi
authors.forename: Wan-Cherng
authors.initials: WC
authors.lastname: Perng
authors.forename: Kun-Lun
authors.initials: KL
authors.lastname: Huang
mesh_terms: D000818:Animals; D001831:Body Temperature / Q000502:physiology*; D001833:Body Temperature Regulation / Q000502:physiology*; D007035:Hypothermia / Q000276:immunology / Q000503:physiopathology; D015227:Lipid Peroxidation / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008171:Lung Diseases / Q000209:etiology / Q000276:immunology / Q000503:physiopathology*; D008297:Male; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000150:complications / Q000276:immunology / Q000503:physiopathology*
chemical_list: D008070:Lipopolysaccharides