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.
The objective of the present study was to evaluate the structural changes in the capillaries, arterioles, venules, and cardiomyocytes in the myocardium of the rats following the craniocerebral injury (CCI). Eighteen non-pedigree white female rats with the craniocerebral injury were used as the CCI model. All the animals were given an intraperitoneal injection of sodium thiopental (100 mg/kg b.w.) within 3, 7, and 12 days after the injury. The heart was removed after thoracotomy and the myocardial tissue was examined with the light and electron microscopes. It was shown that the rats with the craniocerebral injury developed well apparent changes in the myocardial tissue during the early post-traumatic period that affected not only the blood vessels themselves (capillaries, arterioles, venules) but also the intra- and extravascular structures. Changes in the microcirculatory system included damages to the mitochondria, myofibrils, cell nuclei, sarcoplasmic reticulum, and cardiomyocytes. It is concluded that the morphological changes in the myocardium of the animals associated with the craniocerebral injury can induce the development of functional disorders in the cardiovascular system during the early post-traumatic period.
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