Evaluation of the Content of Aquaporin-5 and Epithelial Sodium Channel in the Lungs of Rats during the Development of Toxic Pulmonary Edema Caused by Intoxication with Acylating Pulmonotoxicants.

We studied the content of aquaporin-5 (AQP₅) and epithelial sodium channel (ENaC) in rat lungs during the development of toxic pulmonary edema (TPE) caused by intoxication with phosgene and perfluoroisobutylene (1.5 LC₅₀). The lung body weight index (LBI) was calculated and histological examination of the lung tissues was performed. Localization and expression of AQP₅ and ENaC were determined by immunohistochemistry. Intoxication led to a significant (p<0.05) increase in LBI and histological changes typical of TPE 1 and 3 h after the exposure. In 1 and 3 h after phosgene intoxication, the AQP₅ and ENaC content significantly (p<0.05) increased in comparison with the control. Similar changes in the AQP₅ and ENaC content were observed 1 and 3 h after exposure to perfluoroisobutylene. It was hypothesized that AQP₅ plays an important role in the formation of TPE caused by intoxication with acylating pulmonotoxicants. An increase in the content of ENaC can be considered as a compensatory reaction of the body aimed at clearance of the alveolar fluid. [ABSTRACT FROM AUTHOR]