The effects of hypothermia on endotoxin-primed lung

Hypothermia may be effective for endotoxin-induced acute lung injury. In most studies, hypothermia was induced before the development of neutrophilic inflammation, which would be clinically irrelevant. We investigated whether hypothermia induced after the onset of such neutrophilic inflammation reduces acute lung injury.

In the first experiment, rats were allocated to one of four groups: intratracheal saline instillation/killed at 1 h (saline), intratracheal lipopolysaccharide (LPS) instillation/killed at 1 h (LPS-primed), intratracheal LPS instillation/killed at 6 h (LPS-NT), all under normothermia (NT) (37 +/- 0.5 degrees C) throughout study, and intratracheal LPS instillation/killed at 6 h with hypothermia (HT) (32 +/- 0.5 degrees C) for the last 5 h of study (LPS-HT). Lungs were lavaged for biochemical measurements. In the second experiment in 26 additional rats, we followed exactly the same protocol as described above for the saline group (n = 2), LPS-NT (n = 12), and LPS-HT (n = 12), and obtained a fresh pool of alveolar neutrophils to assess oxidative burst.

Compared with the LPS-primed group, the neutrophil count, protein level, and lactate dehydrogenase activity in the bronchoalveolar lavage fluid, and myeloperoxidase activity of the lung were all higher in the LPS-NT group. Compared with this LPS-NT group, the neutrophil count, protein level, and lactate dehydrogenase activity in the bronchoalveolar lavage fluid, and microscopic scores for alveolar neutrophilic infiltration were all lower in the LPS-HT group. The stimulated production of hydrogen peroxide in neutrophils was lower in the LPS-HT group than in the LPS-NT group.

Hypothermia, applied even after the onset of neutrophilic inflammation, was effective in reducing endotoxin-induced acute lung injury.