The investigation object: patogenesis the hypostatic pneumonia arising on background chronic insufficiency of blood circulation. The investigation goal: clarification of immunological and prooksidantno-antioxidant mechanisms hypostatic pneumonia arising owing to chronic insufficiency of blood circulation, and as justification of new principles of its prevention and treatment. Methods of research: immunological, biochemical, histologic, histochemical, immunohistochemical, pharmacological, clinical, statistical. Theoretical and practical value of the obtained results. Dissertational work belongs to basic researches. The received results expand and deepen existing ideas of mechanisms of hypostatic pneumonia and matter for development of the general pathology of an inflammation and improvement of principles and methods of pathogenetic antiinflammatory therapy. Scientific novelty of the obtained results: For the first time the special complex research devoted to clarification of cellular and humoral, specific and nonspecific immunological and prooxidant-antioxidant mechanisms of hypostatic рneumonia, arised on background chronic insufficiency of blood circulation. Conformities to law and features of morphofunctional are set, including immunohistochemical, changes in the peripheral (spleen, lymph nodes) links of the immune system and in tissue of lungs at a chronic heart failure(CНF) without hypostatic pneumonia and with з by her presence. It is shown, that in the process of chronic cardiac insufficiency formation, obviously because of increased circulatory hypoxia, there is permanent activation of lipid peroxidation on a background of antioxidant system reserve exhaustion that leads to development of secondary immunological insufficiency. The latest leads to a gradual change of nonspecific immunity: decrease in functional activity of PMNL and complement, and increase in contents of pro-inflammatory cytokines and CRP; activation of humoral specific reactions which is obviously a result of tissue damage and autoimmunization of the оrganism; inhibition of specific cellular immunity (decrease in T-helper activity and increase in suppressor one). Immunological insufficiency promotes to infection joining and hypostatic pneumonia development, which, in turn, is characterized by further lipid peroxidation, macrophage and В-cellular links of immunity activation and Т-cellular link of immunity suppression. Additional use of immunomodulators and antioxidants to the generally accepted therapy results in the increased activity of antioxidant system, reduced intensity of lipid peroxidation and immunological changes both in pneumonia and in CHF without pneumonia. It confirms the pathogenetic meaning of found immunological and prooxidant-antioxidant changes at these complications and grounds the early inclusion of immunomodulators and antioxidants in the complex therapy of hypostatic pneumonia complicated СНF and CHF without pneumonia. The degree of implementation: Kharkiv National Medical University, N.I. Pirogov Vinnitsa National Medical University, Gorky Donetsk National Medical University, Odessa State Medical University, S.I. Georgievsky Crimea State Medical University, Lugansk State Medical University, I.Y. Gorbachevsky Ternopil State Medical University, Sumy State University.
