Abstract
The aim of the study is to determine the nature of the consequences of non-respiratory lung function disorders and their influence on the hemostatic system in chronic inhalation of industrial hydrogen sulfide gas (HS). There were studied the parameters of hemostasis system (the number and function of platelet, total clotting time, level of soluble fibrin-monomer complex and D-dimer, speed of XIIa-dependent euglobulin lysis, the activity of Willebrand factor and factors VIII, protein C and inhibitor of tissue plasminogen activator-1 (TPA-1), the content of antithrombin III and plasminogen) in 146 white laboratory male rats taking into account the artery-venous difference. Blood collection was carried out from the abdominal aorta (pars abdominalis aortae) ("after the lungs") and from the posterior vena cava (vena cava caudalis) ("to the lungs", that excludes the influence of the liver). The rats were divided into 9 groups: four groups were experimental, which were exposed to HS for one month (20 animals), two months (20 animals), three months (19 animals) and four months (19 animals). HS was fed into chambers at a concentration of 70±2.34 mg/m3 by static method (once). Inhalation of rats with gas lasted for 4 hours a day, 5 days a week. The control groups were rats placed in cells with a normal air composition in a similar mode for a period of one, two, three and four months (12 individuals each). The reference parameters of the hemostatic system were determined before the experiment in a group of 20 rats. It was found that the artery-venous difference in the indicators of soluble fibrin-monomer complex (p<0.05), the content of antithrombin III (p<0.05), the activity of protein C (p<0.01) is more pronounced in the groups of the 1st month of exposure to HS. Increased activity of platelets (p<0.05), of Willebrand factor (p<0.05) and TPA-1 (p<0.001), as well as slowing of fibrinolysis (p<0.05) indicates the damage to the endothelium of pulmonary capillaries by the 4th month of HS inhalation and the decrease of ability of the lungs to regulate hemostasiological balance.
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