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G Ia Levin

Publications and source records attributed to G Ia Levin.

At least 37 records · Page 2Linked to original sources
PubMed1980

[Effect of trypsin on intravascular erythrocytes aggregation].

The role of proteolytic enzymes in intravascular aggregation of red cells was studied in experiments on rats by intravital microscopy. Intravenous injection of trypsin (40--50 mg/kg) combined with heparin (1000 units/kg) produces marked intravascular aggregation of red cells. Preliminary infusion of pentoxyphyllin (20 mg/kg) or acetylsalicylic acid (100 mg/kg) blocked this process. A conclusion is made about an important role of proteolytic enzymes play in the development of microcirculatory disorders. A possible mechanism of the aggregating action of trypsin and approaches to its correction are discussed.

Animals↗
PubMed1980

[Effect of acetylsalicylic acid and pentoxifylline (trental) on intravascular erythrocyte aggregation stimulated by arachidonic acid].

The role of arachidonic acid (3--5 mg/kg animal body weight) in the intravascular red cell aggregation was studied on rats by intravital microscopy. It has been established that intravenous injection of arachidonic acid leads to aggregation and red cell hemolysis, and animals' death. Preliminary injection of acetylsalicylic acid or pentoxyphylline prevents the initiation of aggregation and lysis of red cells but does not avert the animals' death because of arachidonic acid. It is concluded that arachidonic acid plays an important role in aggregation and lysis of red cells. It is recommended that reasons for animals' death because of arachidonic acid in the absence of microcirculatory disorders be studied.

Animals↗
PubMed1977

[Refractory nature of erythrocytes and thrombocytes].

The authors studied the influence of proteolytic enzymes and arachidonic acid on the erythrocyte and platelet aggregation. These substances stimulated the blood formed elements aggregation. At the same time preliminary incubation of fibrinolysin, trypsin and arachidonic acid with the blood formed elements suspension was accompanied by a significant reduction of their aggregation capacity, i.e. by the development of a refractory condition. A possible mechanism of this phenomenon is discussed.

Adenosine Triphosphatases↗
PubMed1977

[Role of prostaglandin endoperoxides in thrombocyte aggregation].

Phospholipase A and lysolecithin stimulated the thromboplastic factor release reaction and the red blood cells and platelets aggregation. According to polarographic research data, these aggregating agents brought about oxygen consumption in the platelet-containing medium. In all probability, this indicated that endoperoxides, an intermediate product of prostaglandin synthesis, were created under the mentioned conditions. Albumin failed to prevent the oxygen release reaction and its consumption, provoked by phospholipase A and lysolecithin, but totally inhibited their aggregation capacity. On the contrary, aspirin, blocked the oxygen consumption by platelets, without producing any significant effect on the lysolecithin aggregation capacity. It is assumed that the blood formed elements aggregation is due to perturbation of their membrane lipid-protein structure, and not to the endoperoxide synthesis.

Albumins↗
PubMed1976

[Effect of phospholipase A on erythrocyte and thrombocyte aggregation].

A study was made of the effect of plasmin and trypsin on the phospholipase activation, and also of the action of phospholipase A (cobra venom) on the release reaction and the erythrocyte and thrombocyte aggregation. Trypsin and fibrinolysin proved to activate phospholipase, this being accompanied by the accumulation of nonesterified fatty acids in the blood serum. Phospholipase A caused a release of the thromboplastic factor from erythrocytes and thrombocytes and their aggregation. The later is inhibited by albumin and EDTA. It is suggested that the action of the proteolytic enzymes on the blood formed elements was realized through the phospholipase activation.

Catalysis↗