Hemostasiological profile in rats under single exposure to submaximal and maximum hypercapnic hypoxia

Hypoxia is the main link in the taxis pathogenesis to most extreme factors. It occurs in many pathological processes. The aim of the work was to study the hemostatic system in rats under a single exposure to submaximal and maximum hypercapnic hypoxia. Materials and Methods. The experiment enrolled 40 Wistar male rats. Single 20-minute hypercapnic hypoxia (HH) was modeled by placing the animals into a chamber with a gas mixture: submaximal HH: O2 - 9 %; CO2 -7 %; maximum HH: O2 - 5 %; CO2 - 5 %. Results. Single submaximal HH was accompanied by a decrease in the platelet number under a constant level of their aggregation activity. Hypercoagulable shift was observed along the internal pathway and at the final stage of coagulation against the decrease in fibrinogen concentration. AT III level decreased, however, there were no changes in blood APR. Single maximum HH led to more pronounced coagulable shifts. Platelet hemostasis responded by a decrease in the platelet number with a simultaneous increase in their aggregation activity. As for coagulation hemostasis, hypercoagulation was recorded at all stages of coagulation. At the same time, fibrinogen concentration in blood plasma decreased, and the level of soluble fibrinmonomer complexes (SFMCs) significantly increased. The authors reported an increase in plasma fibrinolytic activity. Conclusion. Thus, upon a single exposure to submaximal HH, hypercoagulation was not yet accompanied by thrombinemia markers. At the same time, the danger of thrombotic state development remained, since the hypercoagulable shift was recorded against a decrease in blood plasma anticoagulant activity. A further increase in HH intensity was accompanied by deteriorating hemostatic functions of experimental animals, which could be described as a state of thrombotic readiness. A decrease in the anticoagulant level in response to maximum HH exacerbated thrombosis risks.