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The purpose of this study is to evaluate the validity of the classical model of DIC-syndrome in the conditions of tissue factor initiation. The study was performed on 60 male mice. All laboratory animals were divided into two groups: the first group of mice used a mixture of solutions of 0.5 mg/kg of collagen and 0.06 mg/kg of epinephrine as a trigger for thrombosis, the second group – 10 mg/kg of recombinant tissue factor. In conditions of systemic thrombosis, injected suspension of epinephrine and collagen (group I) resulted in the death of all animals within 3 days. Notably, more than 50% of the mice died within the first hour of the experiment. The death rate in group II on the 14th day of the experiment was 100%, but in contrast to group I, the death of laboratory animals was registered daily throughout the entire observation period (2.0±1.8 vs 133.5±124.7, p<0.01). The results show uniform loss in laboratory animals after induction of thrombosis, and morphological evaluation of animals is characterized by a low content of blood clots in the lungs of lab animals, suggesting the root cause of death of animals is not in acute thrombosis but in the development of delayed manifestations of DIC, which this model does not presuppose since it is designed to evaluate the effectiveness of new antiplatelet drugs in the acute experiment. Thus, the findings demonstrate the limitations of the use of tissue factor in model thrombosis and justify the feasibility of using physiological aggregation inducers.

DIC MODEL ON MICE. TISSUE FACTOR OR PLATELET AGGREGATION INDUCERS?