Because ventilator-induced lung injury is partly dependent on the intensity of vascular flow, we hypothesized that hypothermia may attenuate the degree of such an injury through a reduced cardiac output.

Twenty-seven male Sprague-Dawley rats were randomly assigned to normothermia (37±1℃)-injurious ventilation (NT-V) group (n=10), hypothermia (27±1℃)-injurious ventilation (HT-V) group (n=10), or nonventilated control group (n=7). The two termal groups were subjected to injurious mechanical ventilation for 20 min with peak airway pressure 30cm H₂O at zero positive end-expiratory pressure, which was translated to tidal volume 54±6ml in the NT-v group and 53±4ml in the HT-V group(p>0.05).

Pressure-volume(P-V) curve after the injurious ventilation was almost identical to the baseline P-V curve in the HT-V group, whereas it was shifted rightward in the NT-V group. On gross inspection, the lungs of the HT-V group appeared smaller in size, and showed less hemorrhage especially at the dependent regions, than the lungs of the NT-V group. [Wet lung weight(g)/body weigh (kg)] (1.6±0.1 vs 2.4±1.2 ; p=0.014) and [wet lung weight/dry lung weight] (5.0±0.1 vs 6.1±0.8 ; p=0.046) of the HT-V group were both lower than those of the NT-V group, while not different from those of the control group(1.4±0.4, 4.8±0.4, respectivyly). Protein concentration of the BAL fluid of the HT-V group was lower than that of the NT-V group(1,374±726 ug/ml vs 3,471±1,985 ug/ml;p=0.003). Lactic dehydrogenase level of the BAL fluid of the HT-V group was lower than that of the NT-V group(0.18±0.10 unit/ml vs 0.43±0.22 unit/ml;p=0.046).

Hypothermia attenuated pulmonary hemorrhage, permeability pulmonary edema, and alveolar cellular injuries associated with injurious mechanical ventilation, and preserved normal P-V characteristics of the lung in rats.