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1.
Biull Eksp Biol Med ; 99(5): 578-80, 1985 May.
Article in Russian | MEDLINE | ID: mdl-4005412

ABSTRACT

It was established in experimental normobaric and hypobaric hypoxia and hemic hypoxia induced by carbon monoxide poisoning that zinc compounds administered in a dose of 0.15 mA/kg have a marked prophylactic protective effect. The mechanism of action of zinc compounds consists in changes of oxygen transport blood function. It was shown that interaction of the hemoglobin molecule with zinc ion brings about an increase in Hb affinity for O2 (the left drive of the oxyhemoglobin dissociation curve), a reduction in cooperative interaction of hemoglobin subunits, and a relative decrease in hemoglobin affinity for carbon monoxide. The leading defence mechanism against hypoxic hypoxia is the left drive, the mechanism of defence against carbon monoxide protection consists in the lowering of the "hem-hem" cooperation and of the relative hemoglobin affinity for carbon monoxide.


Subject(s)
Hypoxia/drug therapy , Zinc/therapeutic use , Acute Disease , Altitude , Animals , Atmosphere Exposure Chambers , Carbon Monoxide Poisoning/blood , Carbon Monoxide Poisoning/complications , Carbon Monoxide Poisoning/drug therapy , Carboxyhemoglobin/analysis , Drug Evaluation, Preclinical , Hypoxia/blood , Hypoxia/chemically induced , Male , Mice , Oxyhemoglobins/analysis , Potassium Cyanide/toxicity , Rats
3.
Farmakol Toksikol ; 41(4): 480-2, 1978.
Article in Russian | MEDLINE | ID: mdl-668876

ABSTRACT

Intraperitoneal injection of a 1-sodium fluoride solution (35--40 mg/kg) to male rats was seen to cause a 8--9 fold rise of the blood histamine content and to significantly lower the oxygen tension in the musculus femorins. Preliminary administration of diprazine (5 mg/kg) prevented the death of the animals and lowered the degree of oxygen deficiency in the tissues. An interference is drawn on the important pathophysiological role played by an increase of the histamine content in the blood of the animals in the mechanism underlying the development of circulatory hypoxia in acute poisoning with sodium fluoride.


Subject(s)
Fluoride Poisoning , Hypoxia/chemically induced , Sodium Fluoride/poisoning , Animals , Histamine/blood , Hypoxia/physiopathology , Hypoxia/prevention & control , Male , Muscles/physiopathology , Oxygen/physiology , Pressure , Promethazine/pharmacology , Promethazine/therapeutic use , Rats
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