The purpose of this work is to study the causes and mechanisms of the development of mixed hypoxia in patients with multiple injuries and to consider the possibilities of pharmacological correction. Shock as a form of adaptation of an organism to extreme conditions of existence, was formed on the basis of both passive and active defense reactions. About the physiological sense of initial reactions is a peculiar revaluation of blood flow, which characterized the energy demands of different systems of the organism. Completely different changes occur when the active forms of protection fail. Generally, the stimulation of system activity in most cases varies with their oppression. Among the nonspecific protective mechanisms included in shock at different levels (systemic, regional, tissue), include: centralization of blood circulation, hypothermia, stimulation of anaerobic oxidation. Based on the analysis of the literature, we considered the development of the state of tissue hypoxia in the conditions of traumatic injury. Aerobic oxidation and oxidative phosphorylation in mitochondria process is decreased and leads to the decrease of the amount of ATP, the increase of the content of adenosine diphosphate (ADP) and adenosine monophosphate (AMP). The decline in the ATP/ADP+AMP coefficient and activation of the phosphorfructokinase enzyme (PFK) is the cause of increase in the anaerobic glycolysis reaction, decrease in the functional capabilities of the cell and the development of tissue hypoxia. The number of adaptive reactions includes changes in the blood system and tissue processes, one of which is an increase in 2,3-DFG in red blood cells, that leads to reduces the affinity of hemoglobin for oxygen. The number of adaptive reactions includes changes in the blood system and tissue processes, one of which is the increase in 2.3-DFG in red blood cells, that leads to reduces the affinity of hemoglobin for oxygen. The state of hemorrhagic shock, and the associated haemic type of hypoxia, requires urgent correction by blood transfusion. It is known that during long-term storage of red blood cells there is a loss of ATP and 2.3-DFG, as well as a blockade of the cellular mechanism for the release of ATP because of deforming effects on cells in trauma. It is possible that a deficit of 2.3 DFG is caused by both mechanisms: the total loss of red blood cells during blood loss, and the deposition in the areas of impaired microcirculation. The problem of lack of energy compounds and phosphorus-containing substrates creates the need for additional intensive therapy that affects the metabolic processes under conditions of hypoxia of mixed genesis. The use of antihypoxants and antioxidants is reasonable due to the possibility of saving their own macroergic phosphates of cells consumed in the preliminary phosphorylation of hexoses during anaerobic glycolysis.
Full text: PDF (Ukr) 252K