Abstract
We found different associations between disturbances in the brain and heart during compensated and decompensated heart failure. Changes in the content of monoamines (MAs) in the brain at different stages of heart failure (HF) were related to different causes. The increased activity of MA-ergic systems during compensated HF was apparently associated with the functional load that is experienced by the structures of the brain during the development of cerebral processes of autonomic regulation of the compensatory function of the heart. Cerebral hemodynamics in patients with decompensated HF leads to a decrease in the activities of the dopaminergic and serotonergic systems and a permanent mismatch of the central and autonomic mechanisms of cardiac-activity regulation. A functional load test with the administration of dopamine and serotonin precursors revealed unequal MA-synthesizing capabilities of the brain in animals with compensated and decompensated HF. Reduced capacity of the MA-ergic systems during decompensated HF may lead to overwork of the central mechanisms of regulation and the gradual depletion and disruption of compensatory mechanisms, which aggravates the progression of heart failure.
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