Abstract

Objectives: It was to assess vasoprotective effects of ω-3 polyunsaturated fatty acids in cerebral ischemia. Materials and methods: The experiments were carried out on 42 male outbred white rats weighing 260 ± 20 g. modeling of cerebral ischemia was carried out under conditions of intravenous thiopental anesthesia (40-50 mg / kg). The studies used models of subtotal, partial and stepwise subtotal cerebral ischemia. The table shows the experimental groups and the number of animals in them. Subtotal cerebral ischemia (SCI) was modeled by simultaneous ligation of both common carotid arteries (CCA). Partial cerebral ischemia (PCI) was modeled by ligating one CCA on the right. Stepwise subtotal CI (SSCI) was performed by sequential ligation of both CCA with an interval of 1 day (subgroup 1), 3 days (subgroup 2), or 7 days (subgroup 3). To study the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA), animals with CI were injected intragastrically with the drug "Omegamed" (SCI+ω-3 PUFA) at a dose of 5 g / kg body weight for a week. The control group consisted of sham-operated rats of the same sex and weight. Neurological deficits were assessed in the "muscle strength", "swimming test" and "open field" tests after 5-6 hours of the ischemic period. The study was carried out 6 hours after the simulation of the CI. Quantitative continuous data were obtained, which were processed using the licensed computer program Statistica 10.0 for Windows (StatSoft, Inc., USA). Since the experiment used small samples that had an abnormal distribution, the analysis was carried out by methods of nonparametric statistics. Data are presented as Me (LQ; UQ), where Me is the median, LQ is the value of the lower quartile; UQ is the upper quartile value. Differences between groups were considered significant at p <0.05 (Regression Model). Results: With a stepwise bilateral ligation of both common carotid arteries with an interval of 1 day, neurological disorders were most pronounced, which indicates an aggravation of neurological deficit with a reduction in the time between CCA dressings. In rats with SCI, the changes were more pronounced than with PCI, but less than with SCI. The least pronounced changes were noted in the 3rd subgroup (the interval between CCA dressings was 7 days). Studies have shown the dependence of the severity of brain damage in SSCI on the interval between the cessation of blood flow in both CCA. At a 7-day interval between CCA dressings, compensatory mechanisms were activated, which prevented the development of morphological changes and neurological deficits. When CCA was ligated with an interval of 1 day, the degree of neurological deficit was maximal, which indicates insufficient implementation of compensatory mechanisms. Compared with the control group, the rats of the "SCI+ω3-PUFA" group retained neurological deficit, the muscle strength indicator was 86% less (p<0.05), the swimming duration - by 63% (p<0.05), the number of crossed squares - by 55% (p<0.05), the number of washes - by 62% (p<0.05), the number of racks - by 62.5% (p<0.05) and the number of bowel movements - by 60% (p<0.05). However, in comparison with the SCI group, the neurological deficit was less pronounced. There was an increase in muscle strength by 67% (p<0.05), swimming duration by 37.5% (p<0.05) and the number of squares crossed in the open field test by 31% (p<0.05), which indicates the presence of a corrective action in the ω-3 polyunsaturated fatty acids preparation. Conclusion: The introduction of the preparation of ω-3 polyunsaturated fatty acids has a corrective effect in conditions of subtotal cerebral ischemia, contributing to a lesser severity of manifestations of neurological deficit (an increase in muscle strength, duration of swimming and the number of squares crossed in the open field test).

Highlights

  • Acute disorders of cerebral circulation are one of the most pressing problems in modern medicine

  • With a stepwise bilateral ligation of both common carotid arteries with an interval of 1 day, neurological disorders were most pronounced, which indicates an aggravation of neurological deficit with a reduction in the time between CCA dressings

  • At a 7-day interval between CCA dressings, compensatory mechanisms were activated, which prevented the development of morphological changes and neurological deficits

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Summary

Introduction

Acute disorders of cerebral circulation are one of the most pressing problems in modern medicine. The primary mechanism by which stroke causes injury is the focal deprivation of blood flow to the cerebral parenchyma. In atherosclerosis accumulations of fatty material in the arterial subintima amass platelet clumps. These clumps attract thrombin, fibrin, and erythrocyte debris that can coagulate to a size that poses stenotic risk to the cerebral vasculature. Local blood flow stagnation due to low wall shear stress is thought to predispose certain areas of the vasculature, such as the carotid bulb, to atherosclerotic plaque development. The resulting thrombus deprives cells of the cerebral parenchyma of the oxygen they need to function, causing pathology. Plaques can travel to the cerebral circulation from another location, in which case they are called emboli. The heart, by way of atrial fibrillation, is the most common source of these, but they can come from other diseased parts of the arterial system, as well [14, 15]

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