[Experimental characteristics of anthrax intoxication].
In experimental anthrax intoxication, a highly important stage of its pathogenesis consists in microcirculatory disturbances with the phenomena of blood sludge, accompanied by the increased permeability of blood vessels not only for plasma, but also for red blood cells. These disturbances result in perivascular hemorrhages, hemorrhagic infiltrations, edema and cavitary transudates. Pulmonary edema and, as a consequence, the accumulation of fluid in pulmonary alveoli and the respiratory tract are of particular importance and, probably, can be considered the basic cause of the ensuing acute and fatal asphyxia. Such vascular and pulmonary insufficiency is accompanied by a decrease in the content of macroergic compounds (and in particular ATP), the characteristic deformation of red blood cells and disturbances in their oxygen transport function, which is linked with the decreased content of 2,3-diphosphoglycerate.
D019794:2,3-Diphosphoglycerate; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000097:blood; D000818:Animals; D000881:Anthrax / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D000942:Antigens, Bacterial; D001408:Bacillus anthracis; D001427:Bacterial Toxins / Q000633:toxicity; D004247:DNA / Q000378:metabolism; D004163:Diphosphoglyceric Acids / Q000097:blood; D004912:Erythrocytes / Q000378:metabolism / Q000648:ultrastructure; D006651:Histocytochemistry; D008855:Microscopy, Electron, Scanning; D012313:RNA / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D013997:Time Factors
D000942:Antigens, Bacterial; D001427:Bacterial Toxins; D004163:Diphosphoglyceric Acids; C030325:anthrax toxin; D019794:2,3-Diphosphoglycerate; D012313:RNA; D000255:Adenosine Triphosphate; D004247:DNA; D000251:Adenosine Triphosphatases
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