ABSTRACT
Study of ECoG, local cerebral circulation, and brain pO2 in 39 patients in the acute period of severe craniocerebral injury, as well as morphohistochemical measurements around the focus of crushing (in experiments) showed that the transitional zone is a risk zone because the "enzymatic death" of the tissue of this zone occurring at the moment of the injury predetermines extension of the areas of necrosis later on. The most effective measure is the removal not only of the detritus but also of the transitional zone of the focus within the range of tissue that had hardly suffered any changes and the inclusion of vasoactive and dehydration agents in the therapeutic complex.
Subject(s)
Brain Injuries/physiopathology , Brain/metabolism , Cerebrovascular Circulation , Oxygen Consumption , Adenosine Triphosphatases/metabolism , Animals , Brain/enzymology , Brain Injuries/metabolism , Cats , Electroencephalography , Glycerolphosphate Dehydrogenase/metabolism , Humans , Succinate Dehydrogenase/metabolismABSTRACT
Three stages of cerebral metabolism differing in tension were revealed in the acute period of closed craniocerebral trauma. In the mobilization stage (1 hour after trauma) enzymatic reactions reflecting the activity of aerobic and anaerobic glycolysis are sharply intensified. In the resistance stage (from 3 hours to 2 weeks after trauma) stable conversion to anaerobic glycolysis is noted, which leads to marked deficiency in macroergic compounds. Activation of alpha-glycerophosphate, pentose shunt by means of pharmacological agents in combination with hypothermia may be recommended in this stage. In the restoration stage (more than 2 weeks after the trauma) the metabolic processes are gradually normalized and therapy need not be so intensive.