ABSTRACT
The experiment was carried out on 18 rabbits in two experimental groups. Group I: animals with complete 15-min cerebral ischemia infused with PGI2 for 3 min before, during and for 15-min after ischemia. Group II = control: animals with complete 15 min cerebral ischemia. In both groups, cell nuclei of the adrenal cortex were examined. In the 3rd and 6th h after ischemia numerous vesicular structures, intranuclear filaments and granulofibrillar bodies were found in the nuclei. The vesicular structures were enclosed in a single smooth membrane, some combined with the nuclear envelope, others remained independent. Amassing in karyoplasm of vesicular structures, intranuclear filaments and granulofibrillar bodies probably leads to death of the adrenal cortex cell after complete cerebral ischemia. It is suggested that vesicular structures may form as the result of disturbances in the water-electrolyte exchange between cytoplasm and karyoplasm of adrenal cells. In the experimental conditions, PGI2 did not affect the development of irreversible ultrastructural changes in adrenal cortex cell nuclei after complete prolonged cerebral ischemia.
Subject(s)
Adrenal Cortex/ultrastructure , Brain Ischemia/pathology , Epoprostenol/pharmacology , Adrenal Cortex/drug effects , Animals , Cell Nucleus/drug effects , Cell Nucleus/ultrastructure , Electroencephalography , Male , RabbitsSubject(s)
Brain/ultrastructure , Chlorides , Manganese Compounds , Manganese Poisoning , Mitochondrial Swelling/drug effects , Animals , Male , Microscopy, Electron , RatsSubject(s)
Brain Edema/chemically induced , Chlorides , Manganese Compounds , Manganese Poisoning , Animals , Brain/pathology , Brain/ultrastructure , Male , Microscopy, Electron , RatsSubject(s)
Cerebellar Neoplasms/ultrastructure , Medulloblastoma/ultrastructure , Adolescent , Child , Child, Preschool , Female , Humans , Infant , Male , Microscopy, ElectronSubject(s)
Brain Stem/drug effects , Cerebral Cortex/drug effects , Fetus/drug effects , Phenobarbital/adverse effects , Animals , Animals, Newborn , Axons/drug effects , Cerebral Cortex/ultrastructure , Dendrites/drug effects , Female , Maternal-Fetal Exchange , Microscopy, Electron , Pregnancy , Rabbits , Synapses/drug effectsSubject(s)
Brain Edema/etiology , Oxygen/blood , Blood-Brain Barrier , Brain/blood supply , Capillary PermeabilityABSTRACT
The aim of the study was to compare the effect of phenobarbital given to pregnant rabbits and of epileptic seizures on the course of pregnancy, the physical state, and central nervous system development of newborns. Phenobarbital was given orally during whole pregnancy or for the last ten days in amounts 18,5 mg/kg/body weight = 0,1 DL 50. Seizures of "grand mal" type were evoked with electrostimulator every day since the tenth day of pregnancy. Phenobarbital penetrates via placenta, reaches the organs of all fetuses, and seizures provoke hypoxaemia of fetuses. Phenobarbital administered during whole pregnancy exerts an teratogenous effect. Both injurious factors applied after teratogenous period cause a retardation of general development of fetuses. After phenobarbital administration slight brain lesions are visible in the light, electron microscopical and histochemical examination. More evident was the retardation of the development of the central nervous system after both of the examined injurious factors. In the brain stem and in the cortex the neurons are less mature and the synaptic junctions in the cortex are less numerous. In our experimental models phenobarbital seems to evoke more noxious effect than seizures in mothers.
