Hypothermia produces a generalized impact on an organism, with involvement of all organs and systems into the response. It was shown that hypothermia promotes multi-organ dysfunction syndrome, which makes it important to study the influence of hypothermia on condition of hemostasis and microcirculatory systems. Aim. To study the condition of the hemostasis system and the microcirculatory bed in different periods of moderate hypothermia in rats. Materials and Methods. The current study was performed on 50 male Wistar rats. Condition of microcirculatory blood stream in all animals was assessed with laser Doppler flowmetry. Condition of hemostasis system was studied according to routine protocols and an integrated method of examination – thromboelastography. Statistical analysis was performed using Statistica 6.0 software package (StatSoft, USA) with calculation of Mann-Whitney nonparametric test. Results. Analysis of the experimental data showed that moderate hypothermia produced a pronounced modulating influence on the microcirculatory system. Vasodilatation occurred immediately after reaching the stage of hypothermia, suggesting the beginning of decompensation in the experimental animals. The highest risk for hemodynamic pathologies was observed 5 days after cessation of cooling and was characterized by a massive reduction in the vascular tone, intensification of hemodynamics against the background appearance of thrombinemia markers in the blood stream and pronounced inhibition of fibrinolysis. Enhanced hemodynamics of the nutritional vascular bed with the underlying progressive prothrombotic condition is a potent risk factor for thrombosis and multiple organ dysfunction syndrome. Vasospasm that developed 2 weeks after recovery of the body temperature, indicated a profound modulation of vasculature and preservation of high-level sympathetic input, as well as increasing rigidity of blood vessel walls. Rising fibrinogen concentrations confirm a progressive inflammatory reaction. Conclusion. A moderate degree of hypothermia produces a pronounced modulating effect on the microcirculation. The established regularities make it possible to form a clear understanding of the course and development of the pathological reaction in the body of victims and to give recommendations on the use of pharmacological medicine for preventive therapy. Thus, a period has been established when thrombotic readiness is maximal, and use of anticoagulant and antiplatelet drugs is required, together with drugs that improve rheological properties of blood.
Aim. To evaluate the hemostatic effect of fibrin monomer after its intravenous administration at different time periods in experimental trauma. Methods. In the experiments, in a placebo-controlled study, hemostatic and hemostasiological effects of systemic use of fibrin monomer were studied at different time periods after its administration (in 5 min, 1 h and 3 h) in 97 male rabbits of the Chinchilla breed in the controlled liver injury model. Results. A pronounced hemostatic effect was demonstrated for fibrin monomer used at a dose of 0.25 mg/kg demonstrated by a 6.3-fold decrease of blood loss volume (% of circulating blood volume) compared to placebo on the background of the intravenous preventive fibrin monomer administration 1 hour prior to controlled liver injury. Fibrin monomer administration at a stated dose was not accompanied by significant changes in haemocoagulative parameters including measurement of platelet count, activated partial thromboplastin time, prothrombin time, thrombin time, echitox time, fibrinogen concentration, level of soluble fibrin monomer complexes, D-dimer content, and antithrombin III activity. The effect of fibrin monomer is probably realized through some effectors, the nature of which has not yet been studied. The obtained results allow choosing the optimal interval between intravenous administrations of fibrin monomer and controlled liver injury for further study of the mechanisms of its hemostatic action. Conclusion. Fibrin monomer in small doses (0.25 mg/kg) is able to exert a pronounced hemostatic effect with its systemic administration 1 hour prior to the injury without significant changes in haemocoagulative parameters.
Aim. To study the hemostasis system state in rats during hypothermic and post-hypothermic periods. Methods. Male Wistar rats (53 individuals) were used in the study. The animals from the experimental group underwent single immersion cooling in water at a temperature of 5 °C until profound hypothermia was reached, the control group of the animals was placed in water at a temperature of 30 °C. From the animals of the first group, blood was taken immediately after reaching profound hypothermia and from the second group - 24 hours after cooling was stopped. Results. Comparative analysis of the results showed that immediately after the end of a single cold exposure, significant increase in platelet aggregation activity occured, as well as appearance of thrombinemia markers in the bloodstream and inhibition of fibrinolytic system activity. 24 hours after the experimental exposure, these parameters returned to the initial values. When assessing the activity of external and internal ways of coagulation immediately after the termination of cooling, development of hypocoagulation was established, both with routine tests and from thromboelastography. After 24-hour period, hypocoagulation, recorded immediately after reaching the sought rectal temperature, persisted. Thus, after the end of a 24-hour period after cold exposure termination, most of the parameters of hemostatic system that had deviated immediately after the end of the experiment, returned to the normal level. The delayed effect of hypothermia in such cold exposure regimen manifested only by hypocoagulative shift at the initial stages of coagulation. Conclusion. Signs of abnormal hemostasiological blood properties, recorded immediately after the cooling termination, disappear within 24 hours, and only hypocoagulation persists in the blood.
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