ANALYSIS OF THE DYNAMIC OF CHANGES IN CYTOKINE STATUS FOR ACUTE NECROTIZING PANCREATITIS

Background and Aims: experiment studied the features of the dynamics of changes in cytokine status in the development and progression of acute necrotizing pancreatitis. Materials and Metods: Experimental studies conducted on 50 white non-linear rats in which acute pancreatitis modeling carried out by accumulated method (patent № 66667). Determining the level of cytokines (interleukin (IL) - 2, 6, 10 and tumor necrosis factor - α (TNFα) in plasma was performed on the immunosorbent analyzer АИФР - 01 «Униплан» (Russia) with the use of chemicals firm "Biosuorsce" (Belgium). The balance and ratio of various cytokines was evaluated by mathematical definition percent fate of one of the studied parameters in total for all parameters by V.V. Grechenko. Results: detected changes indicates that initiation AP accompanied by active secretion of proinflammatory cytokines "first wave» - TNF-α and IL-6. However, we know that the development of AP primary source of proinflammatory mediators and adhesion molecules is actually acini cells. On the third day since modeling pancreatitis observed a pronounced dominance of pro-inflammatory cytokines over anti-inflammatory. These changes suggest that at this stage of the disease the transformation of the local inflammatory response in the system. This points to the progressive development of SIRS and to determine the stage of development of this AP as "generalized phase inflammatory response." From the third to fifth day there was the development of potentially fatal reactions ( "cytokine explosion"), based on the positive feedback between cytokines and immune cells. That is, the development of SIRS in acute pancreatitis is legitimate, but not fatal reaction to injury. Running the latest development forms the compensatory anti-inflammatory response syndrome (sompensatory anti-inflammatory response syndrome, CARS). With the prolonged progression of ANP and ongoing development of CARS occurs excessive secretion of inflammatory cytokines. The negative effect of the latter is to reduce the functional activity of immune cells. In this situation is completely dysregulation of systemic inflammatory response that can be described as a "mediator chaos." It is obvious that the emergence of this "immune paralysis" accompanied by the development of deep immunosuppression and further deepening manifestations of systemic inflammation. This system promotes generalization of infectious factors, the formation of necrotic suppurative complications and the development of multiple organ failure, all of which determines the outcome of the lethal disease in the later stages of septic process. The above to determine this final stage of inflammation as a "phase of sepsis and multiple organ failure." Conclusion: given the important role of cytokines in the mechanisms of development and progression of acute pancreatitis is pathogenetically justified the use of appropriate methods of influence aimed at correcting cytokine imbalance.