In the work on the experimental and clinical material studied the peculiarities of neutrophil metabolism in acute blood loss. In the available literature, this issue has been studied in sepsis and purulent processes in the body. It is known that neutrophils are characterized by a non-phagocytic type of resistance. This phenomenon consists in the secretion of non-enzymatic cationic proteins (defensins) and leukocyte proteases from the secondary granules of the cytoplasm of neutrophils into the general bloodstream. In severe process, this phenomenon is manifested by a reaction of leukocytolysis, which is manifested by the destruction of the cytoplasmic and nuclear membranes of neutrophils with the release into the bloodstream of nuclear histones and DNA strands. The paper provides reliable data on the activation of the leukocytolysis reaction in peripheral blood flow, both in a chronic experiment on rabbits with dosed blood loss and in acute blood loss in patients with various sources of bleeding. The severity of the leukocytolysis reaction was directly proportional to the severity of blood loss and was evidenced by the degree of neutrophil damage, which was determined by our own method. Indicators of neutrophil damage were normalized by the end of the second week of the posthemorrhagic period. To determine the degree of neutrophil damage, we used our own method of using the cytochemical method of peripheral blood smears with staining of the latter by the method of Pigarevsky VE The results are statistically significant. In the experiment, two series of experiments were performed, in which rabbits simulated 10% BCC blood loss (1st series) and two-volume 25% BCC blood loss (2nd series). The clinic studied the leukocytolysis reaction in 38 patients with acute bleeding of various genesis, urological, surgical, obstetric and gynecological, within 2 weeks of the posthemorrhagic period. The own assumption about possible pathophysiological essence of activation of leukocytolysis at acute blood losses is put forward. Obviously, hypercatecholaminemia in acute blood loss changes the nature of vascular blood flow from laminar to turbulent, and also increases the secretion of non-enzymatic cationic proteins and leukocyte proteases from secondary granules into the bloodstream. With severe blood loss, leukocytolysis is activated, which consists in the destruction of cytoplasmic and nuclear membranes. This releases nuclear histones and DNA strands, which can cause thrombosis in the microcirculatory tract of the body. The process of activation of leukocytolysis in severe blood loss is called suicidal netosis, which leads to immunotrombosis of the microcirculatory tract of the human body. Disruption of microcirculation in body tissues leads to dystrophic and necrobiotic processes in the tissues of internal organs. This is one aspect of changes in neutrophil metabolism in acute blood loss. In addition, acute blood loss, as such, contributes to the ischemia of body tissues, which leads to the formation of small focal necrosis. It is known that the latter can cause a perifocal inflammatory reaction with the release into the general bloodstream of non-enzymatic cationic proteins and leukocyte proteases. NCBs and proteases can cause secondary alteration of human tissues. Endogenous intoxication of an organism that has suffered acute blood loss, nuclear histones of neutrophils, defensins and DNA strands is the basis of multiple organ failure in acute anemia. Therefore, the syndrome of multiorgan failure has a receptor mechanism in the beginning and only over time develop signs of necrosis in somatic cells of the body. Thus, the studies show an intensification of the leukocytolysis reaction, which is manifested by an increase in the degree of neutrophil damage in acute blood loss and normalization of these indicators, ie their approximation to baseline at the end of the second week of the posthemorrhagic period, 14 days after blood loss.
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