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    Natrus L.V., Ryzhko I.N., Kozak A.I., Kryvosheieva O.I., Stechenko L.A.


    About the author: Natrus L.V., Ryzhko I.N., Kozak A.I., Kryvosheieva O.I., Stechenko L.A.
    Type of article Scentific article
    Annotation The article presents an wound burn healing kinetics (7, 14 days) of the skin was studied by ultrastructural methods. The uncorrected hyperglycemia was modeled by streptozotocin on white adult male rats of the Wistar line weighing 180-210 g (n=14), and rats without somatic pathology showed control (n=14). The peculiarities of derma cellular reactions in connective tissue regeneration of the experimental animals have been studied especially carefully. We identified a significant restructuring in the fibroblasts and macrophages structural organization during the electron microscopic study in the rats with burn injury and hyperglycemia. Fibroblasts have a more rounded shape, a small number of outgrowths that are short, and they have signs of delayed differentiation into specialized cells. Macrophages also do not have many outgrowths, have destructively altered cristae and edema of the matrix. The amount of lysosomes is reduced in macrophages, and residual corpuscles with elements of damaged organelles accumulate in macrophages. We detected signs of delayed angiogenesis. Trophic of the dermis tissue is disrupted because of the in the size of the middle shell in arterial-type vessels increases and the glycosaminoglycans formation more intensive. We compiled these data and our data of pathomorphological, histochemical analysis about features of skin regeneration in animals with a burn injury and the disturbance of glucose metabolism. Changing the course of cellular reactions and intercellular interaction during connective tissue regeneration is the cause of impairment and prolongation of wound healing.
    Tags reactions in connective tissue, burn injury, stable uncorrected hyperglycemia
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    Publication of the article «World of Medicine and Biology» №4(62), 2017 year, 157-162 pages, index UDK 616-018.2-091-008.9:[616-001.17+616.153.455-008.61]:57.084.1
    DOI 10.26724/2079-8334-2017-4-62-157-162