Effect of Moderate Hypothermia on the Expression of ICAM-1 in Rat Acute Lung Injury

The purpose of this work is to investigate the effect of moderate hypothermia on intercellular adhesion molecule-1 (ICAM-1) expression in lung tissue in a rat model of lipopolysaccharide-induced acute lung injury (ALI). A rat model of ALI was established by intratracheal instillation of lipopolysaccharide (1.5?mg/kg, 0.5?mL, LPS) 16?h after LPS (1.0? mg/kg ) intraperitoneal administration. Thirty-four male Sprague Dawley rats were randomly divided into 4 groups: control group, receiving saline only; LPS group, receiving LPS; hypothermia group, treated with hypothermia without receiving LPS; LPS+hypothermia group, treated with LPS and cooled to 32.5-33.0℃ when PaO 2/FiO 2 was below 300?mmHg. Hemodynamics and blood gases were recorded every hour. Rats were killed 4?h after ALI, and lungs were taken out for histology and for ICAM-1 immunohistostaining. A visual count of neutrophils per 10 high-power fields (10?hpf) was performed in 10 randomly selected fields per sample in a blinded fashion by light microscopy. PaO 2/FiO 2 was significantly decreased and PaCO 2 was increased in the LPS group as compared with their baseline values. Treatment with hypothermia inhibited the increase in PaCO 2 but had no effect on PaO 2/FiO 2 in the presence of LPS. It was demonstrated that light microscopy of lung samples of animals in the LPS group had significantly higher neutrophil counts when compared with those in the control group ( P <0.01), but moderate hypothermia significantly reduced the neutrophil counts ( P <0.01). In addition, hypothermia reduced the expression of ICAM-1 in lung tissues. Hypothermia significantly inhibits pulmonary neutrophil accumulation and ICAM-1 expression on vascular endothelial cells in the rat model of lipopolysaccharide-induced ALI, which attenuates the lung injuries.