ABSTRACT
In experiments on cats after injection of isothiobarbamine intravenously (50 mg/kg) at 30 min, intracerebral hemorrhage prevented activation of brain glucose utilization, depression of brain oxygen utilization, surplus lactate accumulation in brain, early development of brain edema and death of cats.
Subject(s)
Brain Edema/prevention & control , Brain/drug effects , Carbohydrate Metabolism , Cerebral Hemorrhage/complications , Oxygen Consumption/drug effects , Thiobarbiturates/therapeutic use , Animals , Brain/metabolism , Brain Edema/etiology , Brain Edema/metabolism , Cats , Cerebral Hemorrhage/metabolism , Cerebrovascular Circulation/drug effects , Drug Evaluation, Preclinical , Glucose/metabolism , Lactates/metabolism , Lactic Acid , Time FactorsABSTRACT
Isothiobarbamin injected intravenously to cats in the phase of circulatory hypoxia 1-2 days after intracerebral hemorrhage improves the functional activity, blood supply, oxygen supply to the brain, prevents excessive accumulation of lactate in the brain tissue. The drug exerts the stimulating effect on the disordered local blood flow: the blood supply to the ischemic areas increases, and that of the hyperemic ones decreases. The mechanism of the vasodilative effect of isothiobarbamin is due to inhibition of Ca2+ delivery through the potential-dependent and serotonin-activated channels of the smooth muscle plasmic membrane. The drug activity increases with a rise of the initial vascular tone.