ABSTRACT—Induction of the heat shock response may improve outcome from pathophysiological disturbances. This improvement is associated with and believed to result from expression of heat shock protein (HSP)‐70. Therefore, we examined the temporal expression of HSP‐70 in an animal model of acute respiratory distress syndrome (ARDS) secondary to fecal peritonitis. Specifically, we hypothesize that sepsis in rats impairs pulmonary HSP‐70 expression. ARDS was induced in adolescent rats via cecal ligation and double puncture (2CLP). Sham‐operated animals served as controls. Lung tissue was collected 0, 3, 6, 16, 24, and 48 h after 2CLP and sham operation. Northern blot hybridization analysis was performed to detect steady‐state HSP‐70 messenger ribonucleic (mRNA) levels. HSP‐70 protein levels were determined via immunoblotting and immunohistochemistry. Mortality after 2CLP was 50% at 24 h and 75% at 48 h. Northern blot hybridization analysis revealed no significant change in steady‐state HSP‐70 mRNA levels in lung at any time after 2CLP. HSP‐70 steady‐state mRNA levels increased after sham operation and was higher than values in 2CLP at 6, 16, and 24 h. HSP‐70 protein levels did not change over time in either group. Thus, the expression of HSP‐70 does not change after 2CLP. Although lack of an increase in protein levels may be adaptive after sham operation, it is not appropriate after 2CLP. Therefore, failed HSP‐70 expression represents a form of pulmonary epithelial dysfunction that may contribute to lung injury in sepsis.