Monoamine metabolism in the brain after disruption of cerebral hemodynamics caused by acute blood loss

Abstract

We studied the relationship between neurochemical and functional brain disorders depending on changes in cerebral hemodynamics at different stages of its recovery after acute blood loss. Similar changes in the metabolism of monoamines (MAs) and an increase in seizure susceptibility (SS), which were found at different states of cerebral hemodynamics at 1 hour and 24 hours after hemorrhage, had different causes. In the first case, the changes were mainly due to insufficient cerebral circulation and hypoxia occurring after blood loss, and in the second case, they were due to the prolongation of previous disorders, which continued after the recovery of cerebral hemodynamics. A deficiency of the MA and MA-synthesizing capacity of the brain after acute blood loss extended the duration of functional disorders in the central nervous system, even after the restoration of cerebral circulation.