title: [Reactive changes of the rat brain cellular elements under different conditions of circulatory hypoxia].
abstract: The aim of this study was to detect structural, spatial and quantitative changes of cellular elements of midbrain paranigral nucleus (PNN) and telencephalic anterior cingulate area (ACA) under different conditions of circulatory hypoxia. PNN anteriormedial part and ACA layers V-VI were examined in adult rats 7 days (n=4) after an occlusion of both common carotid arteries as well as in intact (1st control, n=4) and sham-operated animals (2nd control, n=4). In histological the sections, stained with Nissl cresyl violet, and using the methods of glial fibrillary acidic protein and an Ibal-protein detection, the proportions of unmodified, hypochromic, pyknomorphic neurons and ghost cells were determined as well as the numbers of astrocytes, oligodendrocytes, microgliocytes and endotheliocytes. Cell body area of neurons and gliocytes, and the distance between cell bodies and capillaries were measured, a gliocyte-neuronal index was calculated. It was found that brain cellular elements that survive different conditions of a circulatory hypoxia underwent a range of pathological changes. Neurons were in process of nuclear pyknosis, lysis and transformation into the ghost cells. The cells within the hypoxia nuclear zone were prone to death or pyknosis. The neurons located outside the area of hypoxia which were affected only by a humoral impact of reactions of the glutamate-calcium cascade, frequently underwent acute swelling. Microgliocyte reaction in the form of poorly expressed increase in their number and structural signs of activation was an early diffuse manifestation of a prosencephalic focal hypoxia. Endotheliocyte proliferation 7 days after of ischemic challenge was not associated with a chain of cascade reactions and was observed only in the hypoxia focus. Concentration of viable neurons and astrocytes near blood capillaries, as well as an increase in the number of satellite form gliocytes is an adaptation mechanism and a condition for the survival of cells during various types of brain exposure to ischemia.
authors.affiliation: Department of Histology and Embryology, St. Petersburg State Pediatric Medical University, St. Petersburg, Russia
authors.forename: A V
authors.initials: AV
authors.lastname: Droblenkov
authors.forename: N V
authors.initials: NV
authors.lastname: Naumov
authors.forename: M V
authors.initials: MV
authors.lastname: Monid
authors.forename: E I
authors.initials: EI
authors.lastname: Valkovich
authors.forename: P D
authors.initials: PD
authors.lastname: Shabanov
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D002196:Capillaries / Q000473:pathology; D002340:Carotid Artery Diseases / Q000378:metabolism / Q000473:pathology*; D016923:Cell Death; D042783:Endothelial Cells / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D002534:Hypoxia, Brain / Q000473:pathology*; D008297:Male; D008636:Mesencephalon / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D017628:Microglia / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013687:Telencephalon / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D018698:Glutamic Acid; D002118:Calcium