Asunto(s)
Encéfalo/metabolismo , Grupo Citocromo c/farmacología , Metabolismo Energético/fisiología , Hipoxia/tratamiento farmacológico , Inosina/farmacología , NAD/farmacología , Adenosina Difosfato/metabolismo , Adenosina Monofosfato/metabolismo , Adenosina Trifosfato/metabolismo , Animales , Encéfalo/efectos de los fármacos , Combinación de Medicamentos , Metabolismo Energético/efectos de los fármacos , Hipoxia/metabolismo , Hipoxia/mortalidad , Inyecciones Intraperitoneales , Masculino , Ratas , Tasa de SupervivenciaAsunto(s)
Adaptación Fisiológica , Encéfalo/metabolismo , Hipoxia/fisiopatología , Mitocondrias/metabolismo , Fosforilación Oxidativa , Animales , Encéfalo/enzimología , Encéfalo/fisiopatología , Transporte de Electrón , Hipoxia/metabolismo , Masculino , Mitocondrias/enzimología , NAD/metabolismo , Oxidorreductasas/metabolismo , RatasRESUMEN
A study was made of the action of the nonsteroidal antiinflammatory agent glucamin on the processes of oxidation and phosphorylation (OP) in isolated mitochondria of the liver. It has been established that glucamin does not exhibit the properties of a separator in the explored concentrations (10(-2)-10(-7) M). Unlike the standard drug voltaren that separates OP processes, it slightly enhances interaction of liver mitochondria which oxidize NAD-dependent substrates. The effect of voltaren is dose-dependent, being pronounced to a greater measure when succinate is applied as a substrate of mitochondria oxidation.
Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Glucosamina/farmacología , Fosforilación Oxidativa/efectos de los fármacos , Animales , Diclofenaco/farmacología , Relación Dosis-Respuesta a Droga , Glutamatos/metabolismo , Ácido Glutámico , Técnicas In Vitro , Masculino , Mitocondrias Hepáticas/efectos de los fármacos , Mitocondrias Hepáticas/metabolismo , Ratas , Succinatos/metabolismo , Ácido SuccínicoRESUMEN
The Fourier spectre of power (SP) and bioelectrical activity of the cortex, hippocampus and hypothalamus were studied in unrestrained rats with high (HR) and low (LR) resistance to oxygen deficiency before and after their stay at the "altitude" of about 11,000 m. After acute hypobaric hypoxia there were the EEG changes in LR rats: displacement of the SP peak in low-frequency activity and decreasing of absolute power of all the ranges of SP. In one hour after the "altitude", these EEG parameters were restored. The EEG of the HR rats was not altered. The cortex of the brain seems to be the most susceptible to hypoxia.
Asunto(s)
Encéfalo/fisiopatología , Hipoxia/fisiopatología , Enfermedad Aguda , Animales , Cámaras de Exposición Atmosférica , Susceptibilidad a Enfermedades/fisiopatología , Electrodos Implantados , Electroencefalografía , Electrofisiología , Análisis de Fourier , Masculino , Ratas , Factores de TiempoRESUMEN
Oxidative phosphorylation parameters have been investigated in the isolated brain mitochondria of rats preliminary divided into non-resistant (NR) and high-resistant (HR) animals by their sensitivity to hypobaric hypoxia. During the NAD-dependent substrates oxidation it was shown that the identical effectiveness of the respiratory chain function in both groups of animals was reached at more tension of the oxidative processes. It has been established that at the identical effectiveness of the succinate oxidation by the brain mitochondria in both groups of animals compensatory potentialities of the succinate-oxidase pathway of oxidation is higher in the brain of the NR to hypoxia animals. It has been shown the regulated influence of the NAD-dependent pathway of oxidation activity on the succinate-oxidase site of respiratory chain. This influence is more expressed in the brain mitochondria of the NR animals that in the HR animals.
