STUDY OBJECTIVES: In this study, we determined the effects of various body temperatures (BTs) after initiation of lipopolysaccharide (LPS)-induced lung injury. DESIGN AND SETTING: Forty-nine, adult, male, Sprague-Dawley rats each weighing 300 to 400 g were used METHODS: The treated rats were challenged with intraperitoneal (IP) administration of 5 mg/kg LPS. Control animals received IP saline solution injections. After 16 h, treated and control animals were anesthetized. The animals received direct intratracheal (IT) injection of LPS (1 mg/0.2 mL) or saline solution (control animals). A cooling or heating blanket was then used to control BT. The rats were randomly assigned to three control groups of mild hypothermia (34 degrees C) plus saline solution, normothermia (37 degrees C) plus saline solution, and mild hyperthermia (39 degrees C) plus saline solution, and three LPS groups of mild hypothermia plus LPS, normothermia plus LPS, and mild hyperthermia plus LPS, where each condition was maintained for 5 h. The mean arterial pressure (MAP) and blood gas concentrations were measured. BAL was done in the left lung 5 h after the IT injection of LPS with temperature control. Parts of the right lung were excised for myeloperoxidase (MPO) and malondialdehyde (MDA) measurements, whereas the rest was collected for wet/dry (W/D) ratio determination. RESULTS: Normothermia plus LPS caused significantly increased W/D ratio, LDH activities, protein concentrations, and tumor necrosis factor-alpha concentrations in BAL fluid, and MPO activities and MDA levels in lung tissues when compared to saline solution control group. MAP and Pao(2) were significantly decreased. The pathologic picture also showed increased neutrophil infiltration in lung tissues. In contrast, treatment with mild hypothermia but not hyperthermia significantly attenuated these parameters when compared with the normothermia-plus-LPS group. CONCLUSIONS: These experimental data suggest that mild hypothermia applied after initiation of acute lung injury induced by LPS in rats had a protective effect by inhibiting the inflammatory reaction.
STUDY OBJECTIVES: In this study, we determined the effects of various body temperatures (BTs) after initiation of lipopolysaccharide (LPS)-induced lung injury. DESIGN AND SETTING: Forty-nine, adult, male, Sprague-Dawley rats each weighing 300 to 400 g were used METHODS: The treated rats were challenged with intraperitoneal (IP) administration of 5 mg/kg LPS. Control animals received IP saline solution injections. After 16 h, treated and control animals were anesthetized. The animals received direct intratracheal (IT) injection of LPS (1 mg/0.2 mL) or saline solution (control animals). A cooling or heating blanket was then used to control BT. The rats were randomly assigned to three control groups of mild hypothermia (34 degrees C) plus saline solution, normothermia (37 degrees C) plus saline solution, and mild hyperthermia (39 degrees C) plus saline solution, and three LPS groups of mild hypothermia plus LPS, normothermia plus LPS, and mild hyperthermia plus LPS, where each condition was maintained for 5 h. The mean arterial pressure (MAP) and blood gas concentrations were measured. BAL was done in the left lung 5 h after the IT injection of LPS with temperature control. Parts of the right lung were excised for myeloperoxidase (MPO) and malondialdehyde (MDA) measurements, whereas the rest was collected for wet/dry (W/D) ratio determination. RESULTS:Normothermia plus LPS caused significantly increased W/D ratio, LDH activities, protein concentrations, and tumor necrosis factor-alpha concentrations in BAL fluid, and MPO activities and MDA levels in lung tissues when compared to saline solution control group. MAP and Pao(2) were significantly decreased. The pathologic picture also showed increased neutrophil infiltration in lung tissues. In contrast, treatment with mild hypothermia but not hyperthermia significantly attenuated these parameters when compared with the normothermia-plus-LPS group. CONCLUSIONS: These experimental data suggest that mild hypothermia applied after initiation of acute lung injury induced by LPS in rats had a protective effect by inhibiting the inflammatory reaction.
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