[Changes in energy metabolism parameters of the liver in acute fluoride intoxication and hyperbaric oxygenation].

Examinations of energetic metabolism in liver of white rats with acute fluoride intoxication were carried out in acute and recovering periods. The influence of hyperbaric oxygenation on the change of energetic metabolism indices and on survival rates of animals has been studied. Hyperbaric oxygenation greatly prevented profound metabolic disturbances, in particular, ATP, increased detoxic in liver intensifying energetic forming processes.

[Changes of energy metabolism and concentration of cyclic nucleotides in the kidneys in acute fluoride intoxication and hyperbaric oxygenation].

The energy metabolism and indices of the adenylate-cyclase system in kidneys of rats with acute fluoric intoxication have been studied. It has been determined that the use of hyperbaric oxygenation prevents deep disturbances of energy metabolism in the renal tissue and restricts the increase of adenosine monophosphate concentration. Moreover the survival rate of animals has increased by 30% for the first 24 hours.

[The effect of sodium fluoride on energy and protein metabolism in the rat liver after experimental ischemia].

The experimental study of 88 white rats has stated that peroral introduction of sodium fluoride at a rate of 1.2 mg per 100 g of mass in animals during 3 month period is followed by the development of fluoride intoxication, that causes a considerable decrease of liver resistance to ischemia and more vivid disturbances of its energy and protein metabolism. The activity of the restoration plastic processes after ischemia decreases.

[Dynamics of the plastic processes in the liver during the use of hyperbaric oxygenation in the recovery period following acute massive blood loss].

Acute massive loss of blood lethal for most white rats was induced by blood-letting from the jugular vein (3.5% of the animal mass). The use of hyperbaric oxygenation at 3 atmos (3039 h Pa) immediately after blood-letting for 60 min prevented the depression of RNA and protein synthesis in the liver and the agony development in animals.