Specificity of morphologic changes in target organs, associated with exposure to coal rock dust and fluorine compounds.

The studies revealed specificity of morphologic changes in target organs, depending on acting occupational hazard. Evidences are that inhalation of coal rock dust causes irreversible sclerotic and degenerative changes mostly in lungs and bronchi even on 6th week of the experiment. In liver, changes in parenchyma and stroma are controlled by reparative processes by 9th week. Accumulation of sodium fluoride in the body causes irreversible necrotic changes mostly in liver, on 6th week of the intoxication. With that, morphologic changes in lungs and bronchi are minor, characterized by immune inflammation with degenerative changes only after the 9th week. Irrespective of the acting hazard, vascular changes are characterized by media and intima hypertrophy with endothelial dystrophy and hyalinosis since the 6th week of the experiment.

[Experimental studies of pathogenesis of chronic fluoride intoxication].

The article presents the results of studies of occupational fluorosis pathogenesis on experimental model of chronic fluoride intoxication (CFI). In early fluoride intoxication, fluoride and calcium in the body are in compensatory relations. Later, they are disturbed. High reaction ability of fluoride in CFI is associated with hypocalciemia which triggers parathyroid hyperactivity. This results in hyperproduction of PHH which is unrelated with development of secondary hyperparathyrosis. CFI is accompanied also with elevated calcitonin having a hypocalciemic and hypophosphatemic action. The experiments showed double content of collagen fragments of bone tissue in urine of animals with fluoride intoxication which reflects resorption of bone tissue. Serum osteocalcin rose three-fold as it was unable to include in the bone tissue. There was also activation of lipid peroxidation in subnormal activity of respiratory enzymes.

Disturbances in energy metabolism during traumatic shock and their pharmacological correction.

In compression traumatic shock caused by mechanical crushing of the lower limbs and eventuating in death of 80% animals, hemodynamic disorders by the end of day 1 lead to the development of energy deficiency most pronounced in skeletal muscles and less pronounced in the liver and kidneys. Energy production in the brain and heart was not impaired. Inhibition of ATP synthesis correlated with decreased SOD activity in organs, but not always with activation of lipid peroxidation, which can occur without concomitant disorders in energy metabolism (in the heart and brain). Therapy with succinate-containing hydroxypyridine derivative decreased animal mortality to 10%; this treatment did not modify hemodynamic parameters, but normalized energy metabolism in organs and activity of the antioxidant and prooxidant systems. These findings suggest that tissue (bioenergetic) hypoxia plays an important role in the pathogenesis of compression traumatic shock and that antihypoxic drugs are essential components of therapy of this condition.

[The protective effect of preliminary adaptation to the stress from disorders of the gas-transport function of the blood in hemorrhagic shock]. / Zashchitnyi éffekt predvaritel'noi adaptatsii k stressu ot narushenii gazotransportnoi funktsii krovi pri gemorragicheskom shoke.

To prevent disturbances of blood gas-transport function in hemorrhagic shock, we used cross-over protective effect of adaptation to short-term immobilization stress. Adaptation of rats to stress was associated with a rise in baseline arterial blood, pH in venous blood; fall in PO2, PCO2,P50. Stress-adapted rats appeared more resistant to blood loss. Gas transport 1 hour after hemorrhage was better than in non-adapted animals demonstrated more active compensatory reactions in l low hypoxic damage to the tissues. 2.5-h survival after start of bleeding in control animals made up 35%, in the group of adapted animals--67%. Thus, adaptation to short-term immobilization stress is a non-pharmacological method to prevent hemorrhagic shock.