Reaction of the hemostatic system in response to hypercapnic hypoxia of maximum intensity ­depending on different types of preconditioning

Abstract

Aim. To study the adaptation reactions of the hemostasis system to hypercapnic hypoxia of maximum intensity in rats subjected to preliminary multiple exposure to ethylmethylhydroxypyridine succinate and hypercapnic hypoxia of submaximal intensity.
 Methods. In the experiment, Wistar male rats (80 individuals) were used. Training cycles: 30-fold daily exposure to hypercapnic hypoxia of submaximal intensity (20 minutes — 9.0±0.5% O2, 7.0±0.5% CO2); administration of ethylmethylhydroxypyridine succinate (50 mg/kg) to animals for 30 days; combined effects of the two described modes. Tested experimental exposure was simulated as a single hypercapnic hypoxia of maximum intensity (20 minutes — 5.0±0.5% O2, 5.0±0.5% CO2) at the end of each of three 30-day training cycles.
 Results. Preliminary 30-day exposure to both isolated hypercapnic hypoxia of submaximal intensity and combined exposure to ethylmethylhydroxypyridine succinate contributes to hypocoagulation shift in the hemostasis system and reduces the level of the markers of pre-thrombotic state in response to a single hypercapnic hypoxia of maximum intensity. The state of the hemostasis system after 30-day cycle of isolated use of an antihypoxant is characterized by the inhibition of the vascular-platelet system of the hemostasis system and preserved hypercoagulation shifts in its plasma unit. The obtained results suggest that both preliminary isolated effect of hypercapnic hypoxia of submaximal intensity and the combined effect of hypercapnic hypoxia and ethylmethylhydroxypyridine succinate increase the resistance of the hemostasis system in experimental animals to acute hypercapnic hypoxia of maximum intensity compared to rats of the control group. This was confirmed by the inhibition of the vascular-platelet system, hypocoagulation in the plasma unit, decrease in the level of thrombotic readiness markers and increase in the anticoagulant activity of the blood system compared to the control. At the same time, isolated course administration of ethylmethylhydroxypyridine succinate did not cause the same amount of adaptive changes to maximum intensity hypercapnic hypoxia, since only platelet suppression of the hemostasis and hypocoagulation via the internal coagulation pathway were registered.
 Conclusion. Isolated exposure of hypercapnic hypoxia of submaximal intensity and its combined exposure with ethylmethylhydroxypyridine succinate increase the resistance of the hemostasis system to acute hypercapnic hypoxia of maximum intensity; isolated course administration of ethylmethylhydroxypyridine succinate does not cause the same amount of adaptive changes.