Abstract
The aim. To determine the state of the cerebral vascular endothelium and the role of immunocompetent cells in the ischemic stroke development on the background of atherosclerosis.Materials and methods. We studied cerebral vessels of 50 deaths with ischemic cerebral infarctions, 50 – with severe cerebral atherosclerosis without CVD (cerebrovascular disease) manifestation and 50 deaths, whose cause of death was not related to CVD and atherosclerosis (control group). Histological preparations of vessels were stained with hematoxylin-eosin and Masson Trichrome, and also immunohistochemical study was conducted using CD31/PECAM-1 (Endothelial Cell Marker) Ab-1, CD4 (CD4 Ab-8), CD8 (SP 16), CD20 (CD20 Ab-1) CD68 and (CD68/Macrophage Marker Ab-4) markers.Results. Under ischemic strokes and severe atherosclerosis the cerebral vessels endothelium acquires structural changes in form of rupture, desquamation and exfoliation, formation of desquamated endothelial cells clusters. Speaking of endothelial damage, it should not be supposed that changes should occur at the macroscopic level only, endothelial damage at the cellular level shall be sufficient enough. Immunocompetent cells are of key importance in atherosclerosis development; adhesion on the luminal surface of arteries, presence of a large number of these cells under the endothelium and of more mature macrophages in the intima depth indicates the influx of these cells, which actively potentiate atherosclerosis formation, from the blood into the artery wall.Conclusions. Disorders of the endothelial lining with changes in endothelial cells morphology contribute to the atherosclerotic plaque development. Lymphocytes and macrophages form the molecular basis of many important processes, including the inflammatory response and the immune response
Highlights
Cerebrovascular disorders are one of the leading causes of death in the world
A significant role in the morphogenesis of atherosclerosis is given to the endothelium, which is reflected in the “theory of endothelial damage”, where the cause of atherosclerotic lesions of arteries is defects in the endothelium with platelet adhesion, accompanied by the release of biologically active aggregates
Histological preparations of vessels were stained with hematoxylin-eosin, Mason's trichrome, and carried out immunohistochemical research using markers CD31 / PECAM-1 (Endothelial Cell Marker) Ab-1, CD4 (CD4 Ab-8), CD8 (SP 16), CD20 CD20 Ab-1) CD68 and (CD68 / Makrophager Marker Ab-4)
Summary
Cerebrovascular disorders are one of the leading causes of death in the world. Mortality due to cerebrovascular diseases (CVD) for several decades ranks second in the structure of total mortality. Every 5 minutes one person in Ukraine has a stroke and every 12 minutes one of the patients dies of a stroke; 30-40 % of stroke patients in Ukraine die within 1 month and about half within 1 year, 20–40 % become disabled and only less than 20 % return to full life [1, 2]. These diseases are becoming “younger” and more common every year [3]. Most of them are risk factors for the development of acute and chronic cerebrovascular diseases, and their total effect increases this probability many times over [4, 5]. Macrophages have receptors on their surface for low-density lipoproteins, activation of mononuclear cells through the binding of these receptors to oxidized atherogenic lipoproteins leads to activation of subintimal mononuclear phagocytes, as a result of which they acquire the ability to endocytose lipoproteins
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