The changes of adaptive immune system as a pathogenesis link of crush syndrome

The study of changes of adaptive immunity in the crush syndrome (SDS) is promising because it is pathogenetically reasonable means of immunomodulation of SDS significantly increases the efficiency of therapeutic measures taken in disaster medicine. The aim of the study was to investigate the status of adaptive immunity in an experimental model of SDS depending on the severity of SDS, the serum levels of proinflammatory cytokines and cortisol. The SDS model was reproduced in rats by applying the metal vise with a compressing surface area of 5-6 cm2. The grip was applied at 2, 4 and 6 hours for hind legs under anesthesia tiopentalom and thereby played I, II and III degree of severity of SDS. It is shown that I and II Stephenie the severity of SDS is accompanied by significant (p < 0.05) reduction in the number of leukocytes in the blood and these changes occur against the background of absolute and relative lymphopenia and neutrophilia. Morphometric when I grade SDS in lymph nodes, Peyer's patches, spleen and thymus lymphocyte density significantly higher than in the control group (p < 0.01). At II and III degrees of SDS, the density of lymphocytes is reduced by almost two times, but significantly higher than the values in the control group of rats. Serum levels of soluble CD19 and CD3G due to leddingham of these glycoproteins, and cortisol significantly (p < 0.05) increase in SDS I, II and III severity. Against this background, determined a significant increase (p < 0.05, p < 0.01) the serum level of TNF-a and directly proportional to the severity of SDS. The concentration of IL-6 and if-y also significantly higher than in the control group, however, increasing severity of SDS indicators these cytokines, in contrast, are proportionally decreased. Thus, in an experimental model SDS shown pathogenetically important changes to the system of adaptive immunity. These changes occur in stages according to the severity of SDS and occur on the background of the unmistakable signs of systemic inflammation, as a response to endotoxicosis products rhabdomyolysis, which reaches its maximum at the stage of revascularization of muscle tissue.

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