[The anti-autotoxic immunotherapy of experimental radiation sickness].
A mechanism of formation of autointoxication is described together with the course of rapidly progressing pathology: soon after the injury brought down upon there occur changes in the intercellular fluid protein composition, which are in the nature of things in adaptive processes. Albuminous proteins start appearing, which event suggests to us some deviation from the norm. Such proteins were noted to easily find their way into the blood circulation where they bind with the rest of tissue or blood proteins. This results in formation of protein complexes in the intercellular fluid and blood, with these being not stable in blood for they undergo decomposition with blood coagulation. The above complexes are no longer detectable with deautotoxication using antitoxic serum early after the lethal radiation injury sustained. This is direct evidence in conformation of relatedness of lethal injuries in radiation sickness to complexes of the intercellular fluid proteins. Employment of antiautotoxic sera early in the course of radiation sickness in the experiment to prevent the autointoxication syndrome development makes it possible to derive 100% therapeutic benefit from treatment of lethal injuries with a single AATS injection in a dose of 0.05 ml.
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Fedorych
D000818:Animals; D001327:Autoimmune Diseases / Q000097:blood / Q000209:etiology / Q000276:immunology / Q000628:therapy*; D015551:Autoimmunity / Q000528:radiation effects; D004195:Disease Models, Animal; D007167:Immunotherapy / Q000379:methods*; D051379:Mice; D008810:Mice, Inbred C57BL; D011817:Rabbits; D011833:Radiation Injuries, Experimental / Q000097:blood / Q000150:complications / Q000276:immunology / Q000628:therapy*; D051381:Rats; D017208:Rats, Wistar; D012709:Serum Albumin / Q000032:analysis
D012709:Serum Albumin