Modern possibilities of diagnosis of cell’s membrane-receptor complex dysfunction in the acute period of ischemic stroke

Volodymyr Lychko

doi:10.15587/2519-4798.2020.212710

Abstract

During the development of the acute phase of ischemic stroke (IS), the cytoplasmic membranes of cells and receptor complex are primarily damaged. Structural changes in brain tissue are accompanied by violations of its electric physical characteristics, which are quite qualitatively possible to record using microwave dielectrometry.The aim of the study was to learn the features of changes in the dielectric properties of peripheral blood erythrocytes of patients with IS during in vitro exposure to adrenergic drugs depending on the severity of the disease to optimize diagnosis.Material and methods of research. Measurements of complex dielectric constant (CDC) were performed by EHF dielectrometry at a fixed frequency of 39.5 × 109 Hz, which is in the region of γ-dispersion. The work was based on the materials of a comprehensive examination of 350 patients with the first in the life of IS on the 1st, 10th and 21st day of the disease.The severity of the condition and the degree of neurological deficit were determined using the stroke scale of the US National Institutes of Health (NIHSS) in the first hours of the disease, in the dynamics of treatment on the 10th and 21st day. There were 2 clinical groups: 1st (n = 183) – patients in a state of moderate severity (mean score on the NIHSS scale 11.74±0.33); 2nd (n = 167) – patients with severe IS (average score on the NIHSS scale 24.06±0.29).Results. In the control group, there was a significant decrease after exposure to adrenaline solution. The reaction to adrenaline in patients with IS was almost absent. It indicates a decreasing of erythrocytes β-adrenoceptors (β-ARs) sensitivity to stimulants due to their desensitisation. In patients with moderate severity, erythrocytes are more reactive than in patients with more severe IS.Conclusions. The deviation of CDC of erythrocytes induced by adrenergic drugs in vitro is a manifestation of a specific response of cells to biologically active substances and depends on the functional state of the sympathoadrenal system

Highlights

The cascade of pathological biochemical reactions in the centre of hypoxia during the development of the clinical picture of ischemic stroke (IS) such as oxidative stress, glutamate excitotoxicity, local inflammatory response and others, primarily leads to damage of external cytoplasmic membranes and receptors [1, 2]
Numerous studies show that the work of membrane-receptor complex (MRC) of blood cells reflects the functional state of the whole organism
Results of the research Measurements of complex dielectric constant (CDC) were performed under the influence of adrenaline on erythrocytes of relatively healthy individuals (10-7 M) to identify their response to stress factor with a representation of the relative values of the real part of dielectric constant, which is the difference between the measured CDC before and after exposure to adrenergic drugs (ADs) (Table 1)

Summary

Introduction

The cascade of pathological biochemical reactions in the centre of hypoxia during the development of the clinical picture of ischemic stroke (IS) such as oxidative stress, glutamate excitotoxicity, local inflammatory response and others, primarily leads to damage of external cytoplasmic membranes and receptors [1, 2]. The study of structural and functional changes in the parameters of brain tissue in conditions of acute cerebral ischemia, which correlate with violations of their electrophysical characteristics, opens broad prospects for the use of microwave dielectrometry in angioneurology [3, 4]. This is evidenced by the results of recent studies, which proved the presence of stable changes in the hydrated environment of biological molecules of damaged tissues, which can radically change cell metabolism [5, 6]. One of the most important criteria for assessing is the adrenergic activity of cytoplasmic membranes, which plays a leading role in the pathogenesis of IS [8, 9]

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