A METHOD FOR IMPROVING THE PROFESSIONAL PERFORMANCE AND RELIABILITY OF PERSONS DRIVING HIGH-SPEED VEHICLES.

Recently, due to the emergence of a variety of modifications of air, land, water vehicles and an increase in their speed and maneuverability, the number of people with severe manifestations of motion sickness has also increased. The relevance of this problem is dictated by the fact that, despite significant achievements in the field of preventive medicine, a significant number of people prone to motion sickness have been observed to date. Thus, among persons using land modes of transport, the percentage of sick people reaches 15.

[Using NO-synthase inhibitors derived from L-arginine for preventing acute experimental lung edema development in mice].

The preventive and curative action of NO-synthase inhibitors derived from L-arginine was investigated on the model of toxic lung edema induced by phosgene (LCt50 - 84) in mice. The most pronounced decrease in the phosgene-induced lung edema was observed for aminoguanidine, NG-nitro-L-arginine (L-NNA), and L-nitroarginine methyl ester (L-NAME). Aminoguanidine was effective in cases of both preventive and curative administration.

[Antiedematous effect of diphenyliodinium salts on experimental toxic lung edema].

A series of diphenyliodinium (DPI) salts (chloride, sulfate, acetate and iodide) were synthesized and studied as preventive and therapeutic agents in the model toxic lung edema induced by thiourea and phosgene in rats. All DPI salts exhibited high antiedematous activity. The preventive action of drugs was more effective than their curative effect.

Protective effect of thiazolo[5,4-b]indole in toxic pulmonary edema.

Antiedematous activity of new thiazolo[5,4-b]indole derivatives containing a fragment of isothiourea and characterized by higher antihypoxic activity compared to known antihypoxants was studied on a model of toxic edema of the lungs in mice. Compounds exhibiting high activity on two models of hypoxia (hypobaric and hemic) better protected from lung edema than compounds active only in hypobaric hypoxia.

[Antioxidant system of the rat brain in toxic lung edema].

The state of enzymatic and nonenzymatic components of antioxidant system and also lipid peroxidation processes were studied in brain of rats with toxic pulmonary edema induced by inhalation of nitric oxides. The changes in the state of antioxidant system components in brain accompanied the development of toxic pulmonary edema. The main changes were found in nonenzymatic components of the antioxidant system, particularly in thiol and disulfide groups.