OBJECTIVE

To investigate the effect of hypothermia (HT) on the concentration of surfactant protein A (SP-A) during lipopolysaccharide (LPS) induced acute lung injury (ALI) in rats.

METHODS

Forty male Wistar rats were randomly divided into three groups. The ALI model was reproduced by LPS intratracheal instillation; only saline was instilled intratracheally for control group. Rats in both model group and control group were sacrificed respectively at 1 hour and 8 hours (each n=8). In HT group the body temperature was lowered to 32.5-33.0 centigrade 1 hour after LPS instillation, and 8 rats were sacrificed at 8 hours. The arterial blood gas was determined in all the groups before and 1 hour and 8 hours after instillation of saline or LPS, and the oxygenation index (PaO(2)/FiO(2)) was calculated. The concentration of SP-A in bronchoalveolar lavage fluid (BALF) was determined by enzyme linked immunosorbent assay. The morphological changes in lung tissue of rats were observed under light microscope.

RESULTS

At 1 hour after intratracheal instillation of LPS, the PaO(2)/FiO(2) of each group reached the diagnostic criterion of ALI. Compared with control 1 hour group, the SP-A (μg/L) in BALF of model 1 hour group was decreased (53.27±1.95 vs. 74.81±6.55, P<0.01); the SP-A in model 8 hour group and HT 8 hour group (4.35±2.76 and 51.36±2.33) was both obviously decreased compared with control 8 hour group (70.81±5.01, both P<0.01). Compared with model 8 hour group, the SP-A of HT 8 hour group was obviously increased (P<0.01). Results of light microscopic examination, it was revealed that the alveolar structure of control 1 hour group and control 8 hour group was almost normal. Inflammatory response in lung tissues in model 8 hour group was found to be most serious; compared with model 8 hour group, inflammatory response in lung tissues in model 1 hour group and HT 8 hour group was reduced in certain degree.

CONCLUSION

A certain extent of HT may reduce lung injury of early endotoxin induced ALI rats by delaying lowering of alveolar SP-A levels.