Changes in hemodynamic parameters and abdominal aortic endothelial function in the experiment with prolonged vagotonia

Abstract

The aim of this study was to estimate of hemodynamic reaction and endothelial function on the model of long-term vagotonia.Materials and methods. The studies were performed on 10 hundred-day rats, who were examined by ultrasound scan during ten-day period of vagotonia exposure that simulated the introduction of anticholinesterase drug reversible action of pyridostigmine bromide. The criteria for assessing the type of emerging adaptive response of body changes were indicators of white blood cells. Intraluminal diameter of the vessel, the thickness of the intima – media, endothelium-dependent and endothelium-independent dilation were assessed with ultrasound. In addition, the quantitative characteristics of blood flow: heart rate, peak systolic velocity, end diastolic velocity, resistive index and peak-systolic ‒ frequency/end-diastolic frequency (S/D) ratio were measured. FAQ blood flow rate was calculated according to the formula.Results. It was found that on the background of the model vagotonia stress reaction developed in the body of laboratory hundred-days rats. As a result of analysis of variance hemodynamic revealed some features of the restructuring of the reaction vessel wall, depending on the stage of stress. Thus, stress resistance phase different by violation elastic properties of the wall of the abdominal aorta preserving endothelial function and compensatory capacity of the organism, which included mechanisms to normalize hemodynamics. A stress exhaustion stage was characterized by development of endothelial dysfunction, loss of vascular wall elastic properties and the ability to compensate developing lesions.Conclusions. Studies suggested that in the prolonged vagotonia in healthy individuals puberty long remain compensatory possibilities of cardiovascular system of the body, including the abdominal aorta endothelial, which are included in the normalization of hemodynamic mechanisms. Depletion of compensatory mechanisms coincides with the development of endothelial dysfunction and impaired hemodynamics, partially amenable to targeted pharmacological correction.