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.

[Specificity of cellular response to various occupational toxicants].

The article covers study concerning influence of coal rock dust and high fluorine concentrations on energy metabolism and oxidation-reduction reactions in blood WBC of experimental rats. The authors demonstrated that the cells vary in response to long action of coal rock dust and high fluorine concentrations.

[Tissue morphological changes in experimental anthrasilicosis].

Anthrasilicosis was experimentally stimulated by inhaled inoculation. Various degrees of morphological changes were detected depending on the time of inoculation and the stage of the pathological process: the changes were early observed in the lung and liver, which became worse by week 12 of inoculation; from week 6 these were in the heart and kidney, which was indicative of systemic disorders in response to dust exposure.

[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.

[Using nutriceutics for occupational fluorosis prevention].

The article deals with pathogenesis of occupational fluorosis. Clinical studies demonstrated changes in bone mineral density among workers with 15-20 years of service. Experimental studies proved that occupational fluorosis is associated withcalcium dysbalance,bone tissue resorption and calcium washout. Nutriceutics ("Zolotoi shar", "Korallovy kalcii") in occupational fluorosis play preventive role.

Course of shock in rats with different resistance to shockogenic trauma during Crush syndrome.

Experiments on narcotized rats with crush syndrome showed that low resistant animals developed pronounced hypovolemia, hemoconcentration, blood hyperviscosity, impairment of oxygen metabolism, and central and peripheral hemodynamic disturbances, whereas in highly resistant rats the hemodynamics and oxygen supply to tissues were maintained at a sufficient level, while hemoconcentration and the increase in blood viscosity were less pronounced.