Cerebrovascular diseases (CVD) should be considered as a complex of various neurological, vegetovascular and metabolic disorders, the dynamics of which is mainly stipulated by the degree of vascular insufficiency, cerebral atherosclerosis, blood pressure and risk factors influence [4,5]. One of the most pressing medical and social problems today is the cerebrovascular disease.
The development of acute and chronic cerebrovascular disorders is often preceded by atherosclerosis. These conditions are accompanied by structural and functional changes in the vascular wall, mainly its endothelial lining [2,3,4]. If trigger agents are not neutralised by immunocompetent cells and the inflammatory response progresses, it changes from protective to damaging. Lymphocytes are one of the atheroma components and are mainly localised at the sites of plaque rupture in close contact with macrophages and smooth muscle cells[1,3].
Smooth muscle cells proliferation is positive for atherogenesis, despite the fact that derived from smooth muscle cells macrophage-like cells promote an inflammatory response. Smooth muscle cells are an important component of atherosclerotic formations that ensure the plaque stability. However, smooth muscle cells apoptosis is sufficient for the negative effects of atherosclerosis, such as plaque rupture, inflammation and calcification[2,3,6].
Materials and Methods: we studied 20 cases of death with ischemic stroke on the cerebral vessels atherosclerosis background, 20 cases of death with hemorrhagic stroke on cerebral vessels atherosclerosis background and 20 cases of death not related to CVD and AS (comparison group). We performed immunohistochemical study using the following markers CD4 (CD4 Ab-8), CD8 (SP-16), CD68 (Ab-4), p53 (Clone Y5), Vimentin Ab-2 (Clone V9).
Outcomes
In recent years, the AS origin and development are considered from the standpoint of monoclonal proliferation of smooth muscle cells,immune inflammation and apoptosis. Immunomorphological analysis of the arterial walls showed that, with the exception of the endothelium, all intima and media cells react with antibodies to Vimentin (with ischemic stroke on the background of AS, its expression constituted 59.6 ± 4.8% (p > 0.05) against the total area; in the group with hemorrhagic stroke on the AS background – 52.8 ± 3.7% (p > 0.05), so there is no significant difference in the quantitative content of Vimentin. In the comparison group the expression of Vimentin was 24.2 ± 6.4 (p > 0.05)). We also detected the synthesis of the connective tissue matrix components, i.e. collagen and elastin, which subsequently led to intima thickening and fibrous plaque formation. In the process of atherogenesis in the developed atheroma, along with the smooth muscle cells proliferation we also noted their apoptosis. Smooth muscle cells apoptosis was triggered by proinflammatory factors and took place with the participation of cytotoxic T-lymphocytes (T-killers) therefore in the atherosclerotic lesions focus we registered an accumulation of multitude cytotoxic T-lymphocytes in atherosclerotic lesions constituted 8.56 ± 1.16 (p > 0.05) in the group with ischemic stroke and, respectively, 9.12 ± 1.64 (p > 0.05) in the group with hemorrhagic stroke.
Multitude macrophages contain extensive apoptotic material, which indicates the apoptotic cells phagocytosis. However, the apoptosis development in such macrophages and the presence of multitude apoptotic material extracellularly may indicate insufficient mechanisms of apoptotic cells neutralization in atherosclerotic vascular lesions. In lipid atherosclerotic plaques, apoptotic cells were found both around the atheroma and among the foam cells. Individual apoptotic cells were also localised below the atheroma at the edge of the middle membrane. More pronounced expression of apoptosis p53 marker was observed in the marginal parts and around atherosclerotic plaques.
Conclusions.
1. The number of apoptotic cells increased as the underlying disease progressed. And the intima cells apoptosis is actively involved in atherosclerotic changes development.
2. Increase in the immunocompetent cells number and their apoptosis in the fibrous capsule, reduced number of the fibrous capsule cells, increased proliferation and intense smooth muscle cells apoptosis in atheroma contribute to atheromatous plaque destabilisation and rupture.
3. Apoptosis of macrophages is a useful process for the atherosclerotic plaque stability, provided that there are mechanisms of apoptotic material neutralisation.
References
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2. Bornfeldt KE., Tabas I. Insulin resistance, hyperglycemia, and atherosclerosis. Cell Metab. 2011;14, 575–585 10.1016/j.cmet.2011.07.015 doi: http://doi.org/ 10.1016/j.cmet.2011.07.015
3. Feil S., Fehrenbacher B., Lukowski R., Essmann F., Schulze-Osthoff K., Schaller M., and Feil R. Transdifferentiation of vascular smooth muscle cells to macrophage-like cells during atherogenesis. Circ. Res. 2014;115, 662–667 doi: http://doi.org/ 10.1161 / CIRCRESAHA.115.304634.
4. Mishchenko T.S. Epidemiology of cerebrovascular diseases and organisation of care for patients with cerebral stroke in Ukraine. Ukrainian Bulletin of Psychoneurology, 2017; 25, (90), 22-24.
5. Moshenska O.P. Fatal ischemic stroke: peculiarities of the most acute period. Ukrainian Medical Journal. 2011; 1, (81), 29–35.
6. Rudijanto A. The role of vascular smooth muscle cells on the pathogenesis of atherosclerosis. Acta Medica Indonesiana. 2007; 39(2):86–93
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