Abstract
The global literature constantly receives new data showing the infectious pathogens as factors for development of atherosclerosis and acute cerebrovascular pathology, and the data showing the predictors of pathology of the heart-vessels as markers of inflammation. The results of research about the connection between the infectious agents and atherosclerosis are ambiguous, and the attempts to prove such connection have encouraged the experiments where the infectious agents with atherogenesis are modeled in animals. The connection of this data with ischemic lesion of brain is not properly explored, but certain experimental research show progressive degeneration in brain hemorrhage in mice with herpes virus 1 (HSV1) due to the post-stroke immunosuppression and reactivation of the infectious agent. The aim of this work is to explore experimentally the possible connection between the herpetic infection and the ischemic lesion to the cortex of mice. To achieve this goal we formed 5 groups of experimental animals (mice) for investigation into the possibility of connection between herpes infection and ischemiazaition of brain: 1st group (n=52) - with cholesterol diet; 2nd group (n=23) - with HSV1; 3d group (n=30) - with unilateral occlusion of the common carotid artery; 4th group (n=10) - with HSV1 and occlusion of the common carotid artery; 5th group (n=6) - with cholesterol diet, HSV1, occlusion of the common carotid artery. The microscopic slides evaluated changes morphometrically in the density of the neurons of the neocortex in the ocular of parietal temporal fields of the brain and the hippocampus. The results were processed statistically with Origin Lab 8.0. A probable increase in structural changes was identified in group 5 (with three pathological factors respectively) of the combined model compared to models without association and/or with several pathological signs from the groups 1-4 (1, 2, 3, 4). Comparison of the results between the 1-4th and 5th groups showed a significant increase in the relative number of neurons with cytopathological signs (hemochromatosis, deformation of the perikaryon, karyopyknosis), which may testify in favor of a sufficiently rapid lesion of the pyramidal neocortex neurons influenced by two or more pathological signs. The reduction in the density of pyramidal neurons in the temporal and/or temporal cortex in the combined model with ischemiazaition and viral association in was had greater probability compared to the models formed with only one risk factor. The revealed increase in the degree of neocortex induction during brain cerebral ischemia in mice with herpes infection is an evidence of possible connection between the two.
Highlights
In the world literature, there is a growing number of data indicating some infectious agents, as factors in the development of atherosclerosis (AS) and acute cerebrovascular pathology (ACP), and about the predictors of acute cardiovascular disease as markers of inflammation
The purpose of the work is to investigate in the experiment the possible connection between herpetic infection and ischemic damage to the cerebral cortex of mice
As indicated in the literature, cerebral ischemia in onesided OCCA in mice and rats causes damage to the white matter of the brain, mild motor disorders and memory impairment [27, 31], which is a good model for the study of focal hypoxia [14], vascular dementia and neurodegeneration [29]
Summary
There is a growing number of data indicating some infectious agents, as factors in the development of atherosclerosis (AS) and acute cerebrovascular pathology (ACP), and about the predictors of acute cardiovascular disease as markers of inflammation. The ambiguous results of the research on the relationship between infection and atherosclerosis and attempts to prove the existence of such an association have led to attempts to simulate infection-associated atherogenesis in animals [4, 10, 11, 21]. In the experimental work M.V. Avdeyev and colleagues in 2012 give data on the impact of various infectious agents on the development and progression of Turchyna N.S., Savosko S.I., Ribalko S.L., Starosila D.B., Kolisnik D.I. atherosclerosis [3]. Sorrentino et al (2015) demonstrated the possibility of inducing AS by infection C. pneumoniae in the absence of hypercholesterolemia [25, 26]
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