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Nowadays it is well-known that people with heart failure can have disorders of cerebral hemodynamics, that worsens the prognosis of the disease. However, in the literature there is no common opinion about interconditionality of cerebral blood flow autoregulation and functional heart capacity at different stages of heart failure. Moreover, cerebral hemodynamic disorder in case of heart failure is often a risk factor for seizure readiness increase. Therefore, the research objective is to study the particularities of cerebral hemodynamic autoregulation changes depending on the degree of heart activity decompensation in case of progressing heart failure and to evaluate its relation with the seizure readiness manifestation. The experiments were carried out on white male Wistar rats. To assess the autoregulation of cerebral blood flow the clinical practice uses hypercapnic and compression function tests. These tests activate metabolic and myogenic autoregulation mechanisms respectively. Transcranial Doppler scanning showed no changes in blood flow velocity (Vps and Ved) in basilar artery of animals with CHF and ESD. It demonstrates the absence of cerebral circulation disorders. The animals with CHF did not change their function possibilities of cerebral autoregulation.At the same time, the animals with ESD found to decrease metabolic reserve autoregulation. It testifies slight overstrain of regulation systems. Further aggravation of heart failure leads to progressing decrease of ejection fraction, decrease of VBF in carotid artery and autoregulation reserves. Next we examined what stage of heart failure the seizure readiness begins to increase and whether it is always associated with hypoxia. It was stated that the animals with CHF had the PTZ threshold dose which did not differ from the control group; however the clonic phase was longer. The seizure readiness of the animals with ESD increases by 26%. Thus, in case of ESD the absence of circulatory cerebral disorders associated with an increase in seizure readiness. In case of SSD seizure readiness increased considerably. Our results showed that in case of ESD the decrease of EF and SD does not cause changes in cerebral blood flow in the basilar artery. However, worsening heart failure leads to severe cardiac dysfunction, accompanied by damage to the mechanism of autoregulation. This leads to hypoxic processes that exacerbate the disturbed autoregulation. Thus, we can assume that decreased blood flow in basilar artery in case of severe cardiac dysfunction, due to damage to the mechanism of autoregulation, causes the brain aggravated hypoxic state, which is accompanied by a progressive increase in seizure readiness. In this connection, there is a question conserning increasing seizure readiness amid adequate cerebral blood flow and rather high reserve capacity of autoregulation in animals with ESD. The reason for this may be autonomic imbalance underlying pathogenesis of heart failure. This is confirmed by the published data on the influence of autonomic activity on seizure readiness. Perhaps, the study results allow us to consider that increase in seizure readiness amid adequate cerebral blood flow in ESD is caused not by hypoxia but by neurovegetative imbalance, which appears earlier than the cerebral hemodynamic disorder. The progressive increase in seizure readiness at SSD is connected with the fact that vegetative disorders, arising at ESD, are aggravated by hypoxic-ischemic processes. Thus, the inefficiency of heart at early and severe cardiac decompensation stages unequally affects the reserve capacity of cerebral hemodynamics autoregulation and the level of brain seizure readiness. Moreover, the increase in seizure activity is already apparent at an early cardiac decompensation stage, i.e. amid adequate cerebral blood flow. As the heart failure progresses, there is a significant decrease in cerebral blood flow which leads to aggravating hypoxia and even more expressed than at ESD decrease in seizure readiness. The research results suggest that the increase of brain seizure readiness in case of heart failure is not always caused by hypoxia, but its severity depends on the stage of cardiac decompensation.