Evaluate the role of mercury chloride in the development of toxic pulmonary edema in laboratory animals during intoxication with substances of acylating action

Relevance. Intoxication of acylate pulmonotoxicants causes disturbance of structure and function of air-blood barrier, the output of liquid in the interstitial and alveolar space and manifestation of lung edema. Aquaporins play an important role in the transportation of fluid through the alveolar-capillary membrane, including pathological conditions. Water permeability through aquaporins is blocked by mercury ions. Using mercury chloride may reduce severity of the acute lung edema after intoxication of the pulmonotoxicants.

Intention. The goal is to evaluate the role of mercury dichloride in the development of toxic pulmonary edema in laboratory animals during intoxication with pulmonotoxicants with an acylating effect.

Methodology. Laboratory animals (rats and rabbits) were exposed to inhalation intoxication of carbonic acid dichloride and perfluoroisobutylene at concentrations of 1,5LC₅₀. In 30 minutes after exposure were administrated of 0,3LD₅₀ mercury chloride to the animals subcutaneously. The oxygenation index, acid-base state, pulmonary coefficient, histological changes in lung was investigated in 6 hours after exposure.

Results. It was found that intoxication with carbonic acid dichloride and perfluoroisobutylene at concentrations of 1,5LC₅₀ led to the development of toxic pulmonary edema in rats and rabbits 6 hours following exposure. The administration mercury chloride to 30 minutes following exposure to the pulmonotoxicants under study, led to a decrease (p < 0.05) in the pulmonary coefficient, an increase (p < 0.05) in the oxygenation index and normalization of the acid-base state according to compared with animals receiving 0.9 % NaCl following intoxication. When conducting a histological examination, in animals treated with mercury chloride less pronounced changes in the histoarchitectonics of the lung tissue were noted.

Conclusion. Considering the fact that the administration of mercury chloride to animals led to a decrease in the manifestations of pulmonary edema in animals, it was suggested that aquaporins play an important role in the pathogenesis of toxic pulmonary edema caused by intoxication with pulmonotoxicants with an acylating effect. The use of selective blockers of aquaporins (less toxic than mercury chloride) may be a new direction in the pathogenetic therapy of toxic pulmonary edema due to exposure to pulmonotoxicants.