Abstract

The results of experimental and clinical studies have shown that gipocirculation, hypoxia, acidosis and increased production of free radicals formed by traumatic brain injury cause disruption of the cytoskeleton of endothelial cells and microcirculation in the microvessels of the myocardium. These changes are accompanied by the development of thrombocytopenia. The use of mexicor in the posttraumatic period constrains the intensity of the formation of nonspecific activation of vascular-platelet hemostasis and provides a stabilizing influence on the membranes of endothelial cells, platelets and red blood cells.

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