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Biomedical subjects

L Dydyk

Publications and source records attributed to L Dydyk.

At least 19 recordsLinked to original sources
PubMed1987

Failure of prostacyclin effect on the reversal of early ultrastructural changes in cell nuclei of adrenal cortex after complete 15-min cerebral ischemia in rabbit.

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.

Adrenal Cortex↗
PubMed1979

[Comparison of the transplacental effect of luminal and epileptic seizures in pregnant rabbits on the development of the fetal nervous system].

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.

Anencephaly↗
PubMed1976

Topography of lesions in newborn and infant brains following cardiac arrest and resuscitation. Damage to brain and hemispheres.

The brain lesions produced by temporary arrest of circulation in a newborn and an 11-month-old infant are described. In the newborn, two periods of arrest occurred, one on the fifth day after birth and the second a few day before death on the sixth week. The older infant suffered a single episode of cardiac arrest at the age of 11 months and survived 8 days. In both cases, postmortem examination revealed lesions in spinal cord, in brain stem, and in cerebral hemispheres. This distribution of damage is compared with the patterns of injury produced experimentally by episodes of partial (hypoxia) and total (anoxia) asphyxia in subhuman primates. The coexistence of hemispheral and brain stem nuclear patterns of pathology indicates that both hypoxia and anoxia had occurred in the present cases.

Brain↗