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1 6 , 1 2 ; 5 42 w w w . r e a n i m a t o l o g y . c o mЦель исследования. Оценить роль вторичных факторов повреждения мозга в активации сосудисто тромбоцитарного звена системы гемостаза при черепно мозговой травме (ЧМТ).Материал и методы. В ОРиТ проведено обследование и лечение 30 пострадавших с сочетанной ЧМТ. В посттравматическом периоде у больных исследовали показатели сердечной деятельности и сосудистого то нуса, содержание тромбоцитов, гемоглобина, лактата и активных форм кислорода в крови.Результаты исследования показали, что сопровождающие сочетанную ЧМТ вторичные факторы по вреждения мозга (недостаточность кровообращения, гипоксия, ацидоз и повышенное образование свобод ных радикалов) являются в то же время неспецифическими стимулами тромбоцитов и эндотелиоцитов кро веносных сосудов и, вследствие этого, вызывают системную активацию сосудисто тромбоцитарного звена системы гемостаза.Заключение. Неспецифическая системная активация сосудисто тромбоцитарного гемостаза вторичны ми факторами у больных при сочетанной ЧМТ является одним из патогенетических компонентов ишеми ческого повреждения мозга. Ключевые слова: черепно мозговая травма; сосудисто тромбоцитарный гемостазPurpose of the study. To evaluate the role of secondary brain damage factors in activation of vascular platelet hemostasis in traumatic brain injury (TBI).Material and methods. In the ICU, 30 patients with complex traumatic brain injury were examined and treat ed. In the posttraumatic period, in patient measurement of heart and vascular tone, platelets, hemoglobin, lactate, and active forms of oxygen in the blood were investigated.The study results have showed that damaged brain secondary factors accompanying concomitant TBI (circu latory insufficiency, hypoxia, acidosis and increased free radical formation) represent at the same time nonspecific stimuli for platelets and cells of blood vessels that consequently, cause systemic activation of the vascular platelet link within the hemostasis system.

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The aim of the study was to investigate the effect of ethylmethylhydroxypyridine on the ultrastructural alterations in endothelial cells of liver sinusoidal capillaries (SC) and primary hemostasis in the acute phase of traumatic brain injury (TBI).Materials and methods. Ultrastructural endothelial cell changes were studied in 36 female outbred rats in the acute phase of TBI using electron microscopy, and the platelet count was determined using a blood analyzer. The experimental group (n=18) animals received intraperitoneal injections of ethylmethylhydroxypyridine at the dose of 8.0 mg/kg per day for 12 days, and the control group (n=18) rats were administered with normal saline solution at the same dose.Results. Administration of ethylmethylhydroxypyridine in the early post TBI period reduced microvilli damage in endothelial, hepatic and stellate cells in the Disse space, whereas in the control group a significant decrease of these cells counts was detected. In contrast to the control group, the experimental group animals did not demonstrate thrombocytopenia on the days 1, 3, and 7 after injury. There was a significant increase in the platelet count compared with the baseline values, which was highest on day 12 after injury.Conclusion. Intraperitoneal administration of ethylmethylhydroxypyridine in rats in early post TBI period inhibited the TBI-associated damaging effect of secondary factors on liver sinusoid endothelial cells and platelet consumption.

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