S. M. Kirov Military Medical Academy, Ministry of Defense of the Russian Federation, St. Petersburg, Russia.
State Research Test Institute of Military Medicine, Ministry of Defense of the Russian Federation, St. Petersburg, Russia.
Bull Exp Biol Med. 2022 Sep;173(5):623-627. doi: 10.1007/s10517-022-05600-5. Epub 2022 Oct 10.
We studied the content of aquaporin-5 (AQP) 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 LC). The lung body weight index (LBI) was calculated and histological examination of the lung tissues was performed. Localization and expression of AQP 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 AQP and ENaC content significantly (p<0.05) increased in comparison with the control. Similar changes in the AQP and ENaC content were observed 1 and 3 h after exposure to perfluoroisobutylene. It was hypothesized that AQP 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.
我们研究了在光气和全氟异丁烯（1.5 LC）中毒引起的中毒性肺水肿（TPE）发展过程中，大鼠肺组织中水通道蛋白-5（AQP）和上皮钠通道（ENaC）的含量。计算了肺体重指数（LBI），并对肺组织进行了组织学检查。通过免疫组织化学确定 AQP 和 ENaC 的定位和表达。中毒导致 LBI 显著增加（p<0.05），并且在暴露后 1 和 3 小时出现 TPE 的典型组织学变化。在光气中毒后 1 和 3 小时，AQP 和 ENaC 的含量与对照组相比显著增加（p<0.05）。在暴露于全氟异丁烯后 1 和 3 小时观察到 AQP 和 ENaC 含量的类似变化。据推测，AQP 在酰化性肺毒物中毒引起的 TPE 形成中起重要作用。ENaC 含量的增加可以被认为是机体为清除肺泡液而产生的代偿反应。
