中度低温减轻内毒素性急性肺损伤大鼠肺炎症反应

摘要：Objective To investigate the role of moderate hypothermia in the lung inflammation of rat acute lung injury induced by lipopolysaccharide( LPS). Methods A rat model of acute lung injury (ALI) was established by intra-tracheal instillation of lipopolysaccharide (1.5 mg/kg, 0.5 ml) at 16 h after LPS (1.0 mg/kg) intraperitoneal administration. Thirty-four male Sprague Dawley rats were randomly divided into four groups: control group, receiving saline only;LPS group, receiving LPS; hypothermia group, treated with hypothermia without LPS; LPS + hypothermia group, treated with LPS and cooled to 32.5℃～ 33.0℃ as PaO2/FiO2 was below 300 mmHg. Hemodynamics and blood gases were recorded every hour throughout the study. Rats were killed 4 h after ALI, and lung lavage was performed to measure the tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) concentrations in bronchoalveolar lavage fluid (BALF) by using enzyme-linked immunosorbent assay (ELISA). Results PaO2/FiO2 was significantly decreased and PaCO2 was increased in the LPS group as compared to their baseline values( P 《 0.01 ). Treatment with hypothermia inhibited the increase in PaCO2 ( P 《 0.05) but had no effect on PaO2/FiO2 in the presence of LPS. The administration of LPS significantly increased the concentrations of TNF-α, IL-6 and IL-10 in BALE as compared to the control experiment( P 《0.05, P 《 0.01 ). Moderate hypothermia reduced the expressions of TNF-α and IL-6( P 《 0.01 ) but had no effect on the production of IL-10( P 》 0.05). Conclusion Moderate hypothermia significantly inhibits proinflammatory cytokine expressions in lipopolysaccharide-induced acute lung injury.