Objective:To observe effects of hydrogen sulfide(H2S) intoxication on sodium and water transport function in rat lung and study its mechanism. Methods:SD rats were exposed to H2S gas with semi-lethal concentration(300 ppm) for 3 h. After 6 h,12 h and 24 h exposure to H2S,alveolar fluid clearence(AFC) and wet/dry ratio were measured. HE staining of lung tissues was observed by light microscope,and the change of type Ⅱ alveolar epithelial cells was observed by electron microscope. mRNA expression of α-epithelial sodium channel(ENaC) in the lung tissues was analyzed by real-time PCR. The expression of α-ENaC and ERK1/2 protein in the lung tissue was examined by Western blot . Results:After exposure to H2S, AFC was significantly decreased in SD rats compared to the control group, and reached a lowest level after 6 h and returned to a normal level after 12 h. The lung water content reached a lowest level after exposure for 6 h. Obvious injury changes of the lung tissue of rats were found after exposure for 24 h by light microscope. Dilated mitochondrial cristae and collapsed lamellar bodies were found in typeⅡalveolar epithelial cells of rats after exposure. The expression of α-ENaC mRNA in lung tissue was increased after exposure for 6 h and returned to a normal level after 12 h. Compared to the control group, the protein expression of α-ENaC was significantly decreased after exposure for 6 h. ERK1/2 dephosphorylation in lung tissues was significantly increased after exposure for 6 h. Conclusion:H2S intoxication decreases the AFC of rats and down-regulation of α-ENaC expression may be involved in as a potential mechanism. Furthermore, activated ERK1/2 signaling pathway may participate in the whole damaging process.