RESUMEN
Tests conducted on rabbits in a state of acute ethanol poisoning (2.5 g/kg per os) of a medium degree demonstrated that caffein (10 mg/kg) and bemegride (5 mg/kg) introduced one time intravenously at the height of alcoholic intoxication raise the activity of aerobic oxidative processes, but fail to eliminate metabolic acidosis and do not accelerate the excretion of ethanol. Unlike caffein, bemegride shows a tendency toward respiratory compensation of metabolic acidosis and lowers the activity of the alcohol-dehydrogenase.
Asunto(s)
Intoxicación Alcohólica/tratamiento farmacológico , Estimulantes del Sistema Nervioso Central/uso terapéutico , Equilibrio Ácido-Base/efectos de los fármacos , Acidosis/tratamiento farmacológico , Intoxicación Alcohólica/metabolismo , Animales , Bemegrida/uso terapéutico , Cafeína/uso terapéutico , Evaluación Preclínica de Medicamentos , Humanos , Masculino , Conejos , Factores de TiempoRESUMEN
Experiments on cats under nembutal anesthesia demonstrated that the focus in cerebral cortex with a high level of convulsive activity increases the activity in foci with a low level of convulsive activity, unites them into a functional complex of epileptic activity and determines the behaviour of this complex. Such a focus has been named a determinant. An abolishment of the determinant focus entails a breakage of this complex. The abolishment of any dependent foci fails to produce such effect. The dependent foci are suppressed first of all under ether or halothane anesthesia. Bemegrid injected intravenously revealed first of all the latent determinant foci. The results of such studies as well as some problems of the pathogenesis, diagnosis, therapy and terminology of focal epilepsia are discussed from the point of view of a general conception of the role of the determinant structures in the CNS activity and the theories of generator mechanisms of neuropathologic syndromes characterized by hyperactivity of the systems.