PubMed Health⌕ Search

Biomedical subjects

V A Tumanskiĭ

Publications and source records attributed to V A Tumanskiĭ.

5 recordsLinked to original sources
PubMed1985

[Pathologo-anatomical characteristics of hyperosmolar and other comatous conditions].

Fifty-four cases of death from hyperosmolar comas were examined pathoanatomically together with the postmortem biochemical analysis of the CSF and blood. Brain of animals with disturbances of the blood and CSF osmolarity was studied electron cytochemically and autoradiographically. It was discovered that the hyperosmolar comas are manifested by excosis and brain collapse. The brain is reduced in volume due to deep cell-extracell dehydration and alteration of the hematoencephalic barrier with the irreversible depression of the neuronal and glial metabolism. In 7 patients dying with the purulent-necrotic changes of vessels resulting from the hyperosmolar effect of verografin used for the carotid angiography, numerous perivascular hemorrhages developed in the brain. Dysequilibrium syndrome in hemodialysis is manifested by an acute brain swelling or by a formation at a later period of symmetrical ischemic-hemorrhagic necrosis in the thalamus and occipital lobes of the large hemispheres.

Animals↗
PubMed1984

[Postresuscitation encephalopathy].

On the basis of morphological examination of brain from 250 deceased patients who after clinical death showed, during 1-63 days, symptoms of grave anoxic encephalopathy as well as retrospective analysis of clinical biochemical data, and biochemical post-mortem study of the blood and liquor, the main pathological forms of postresuscitation encephalopathy are distinguished. These are as follows: diffuse-focal anoxic lesions of the brain and spinal cord, partial (complete and incomplete) necroses, isolated total brain necrosis, subtotal necrosis of the brain stem and cerebellum. Morphogenesis as well as extra- and intracranial factors enhancing the development of these forms of encephalopathy are described. Developmental stages of necrotic alterations are singled out, attention is drawn to the processes of organization and reparative regeneration of the brain structural elements in the postresuscitation period. The influence of certain grave metabolic and circulatory disorders on the postresuscitation encephalopathy morphology is shown.

Animals↗