The heat shock protein (HSP) 70 families are known to protect cells against the irreversible tissue injury induced by stress and to induce the recovery of cell function during stress. Heat pretreatment was reported to decrease the acute lung injury(ALI) of rats induced by lipopolysaccharide (LPS). However the role of heat shock with LPS co-treatmenton ALI is unclear. The purpose of this study was to investigate the effect of heat treatment, which was given immediately after the beginning of ALI induced by LPS intratracheally administered in rats.

Either saline (saline group) or LPS was intratracheally instilled without heat treatment (LPS group). In addition, heat was conducted 18 hours prior to the instillation of LPS (pre-treatment group) and conducted immediately after instillation of LPS (co-treatment group). Six hours after the LPS or saline treatment, blood, bronchoalveolar lavage (BAL) fluid and lung tissue samples were obtained. The myeloperoxidase (MPO) activity and the heat shock protein expression in the lung tissue, the differential counts of the polymorphonuclear leukocytes (PMN) in the BAL fluids, and the LDH, protein, IL-1β, TNF-α and IL-10 levels in BAL fluid and serum were measured.

1)The MPO activity, the differential PMN counts in the BAL fluid, BAL fluid and serum cytokines were higher in the LPS, the heat pre-treatment and co-treatment group than those of the saline group (p value <0.05). 2)The MPO activity and the protein level in the BAL fluid from the heat co-treatment group were similar to those of the LPS group. 3) The serum TNF-α level of the heat co-treatment group was significantly higher than that of the LPS group (p=0.01) .

Heat shock response administered immediately after a LPS instillation did not attenuate the ALI in this model.