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Anatolii Arkadevich Pisarev; Lyudmila Vasilievna Anisimova; Irina Ivanovna Fomochkina; Anatoly Vladimirovich Kubyshkin; Dmitry Sergeevich Kuzichkin; Yulianna Ivanovna Shramko; Vladimir Zakharovich Kharchenko; Elena Petrovna Golubinskaya;
Disseminated intravascular coagulation leads to the development of multiple organ failure syndromes with a mortality rate higher than 50 %. We examined the pathogenetic mechanisms of formation of systemic reperfusion syndrome in a rat model of reperfusion syndrome for 6, 12, and 24 hours. A total of 60 white Wistar rats, with a weight of 180–200 g, were studied. We found that morphological changes in the liver were manifested by formation of triggers for hepatocyte damage, including activation of apoptosis and initiation of pro-inflammatory damage pathways. These changes did not lead to severe alterations in functional activity of the liver. Disturbances in the blood coagulation system that developed with reperfusion syndrome with a potential threat of developing DIC were associated with increased consumption of coagulation factors. These disturbances in the blood coagulation system were also associated with inhibition of synthetic function of the liver to a lesser extent.
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Keywords: liver, blood coagulation system, reperfusion syndrome, apoptosis, inflammation