Indexes of endogenous intoxication in experimental burn disease in the stage of toxemia
Journal Title: Naukovyi visnyk Chernivetskoho universytetu. Biolohiia (Biolohichni systemy) - Year 2016, Vol 8, Issue 1
Abstract
Researched thе modeling esophageal alkali burns 2nd degrees in immature rats occurred syndrome of endogenous intoxication. Increased toxins of different nature, specific, and non-specific and mediators of immune responses (increased level of oligopeptides by 34.8% molecule of average weight (MAW) 17%, IL-10 by 4%, and decreased of IL-4 11%), which is associated with high risk of septic complications after burns. We found that the origin of various toxic substances act at all levels of the body. There have come a significant multiple pathological disturbances in the body, namely water-salt metabolism (potassium level increased by 60%, sodium chloride and calcium decreased by 6%, 8% and 19% ), inhibition of the liver and kidney function (reduced total protein, albumin 36.7%, 37%, increased activity of AST, ALT in 21%, 182% and increased levels of urea, creatinine, creatine kinase 92%, 65%, 83%). So antitoxic mechanisms depends on the severity of syndrome endogenous intoxication (SEI). In the normal functioning of the protective mechanisms of the body is able to resist the toxins. In our researches it has been shown that immature rats under 2nd degrees modeling alkaline burn of the esophagus (ABE) protective mechanisms (antitoxic and regulatory system) can not cope in the body and increases the content of endogenous toxins on the background of dysfunction of the immune system leads to lower body resistance. Therefore, it is advisable to immunological and metabolic correction in the treatment of burn patients in the conditions of the esophagus chemical burns of 2nd degrees.
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Indexes of endogenous intoxication in experimental burn disease in the stage of toxemia
Researched thе modeling esophageal alkali burns 2nd degrees in immature rats occurred syndrome of endogenous intoxication. Increased toxins of different nature, specific, and non-specific and mediators of immune respons...
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