Numerous pathophysiologic observations in humans and animals led to the formulation of the response-to-injury hypothesis of atherosclerosis, which proposed that endothelial denu- dation by the blood flow was the first step in atherosclerosis. At present it is impossible to describe hemodynamics only by the Navier-Stokes or Oldroyd-B equations because in the large arteries blood flow is unsteady, with the flow separation and waveform propagation of the thyxotropic mass. The purpose of this paper is to study the impact of the arterial pulse wave on the blood flow and initial factors of atherosclerosis. In 12 healthy men (25-39 years of age) peak velocity, mean velocity, mean flow and net flow in the aorta have been investigated by МR angiography. Initial velocity was registered after 43msec of the ECG-R wave, and it differed from zero at all sites of the aorta, although net flow was equal to zero. Womersley’s number from the ascending to the thoracic aorta decreased from 12.5 ± 1.5 to 7.3 ± 1.2; flow modified from inertio-elastic to viscous. In the aortic arch in protodiastole blood flow separated into the opposite directed streams resulting in wave superposition with the high net flow. At the isthmus area separated waves interferences and reflects to anterograde direction. Here flow acceleration in protodiastole is 6 times higher than in systole. Pulse waves move on artery walls fifteen or more times more rapidly than the blood flow. Pulse oscillation increases strain rate to the contiguous vessel wall flow layers. At the sites with the flow wave negative interference vessel pulse oscillation attenuates and at the boundary reflection flow wave can shift the vessel wall
There is a lot of uncertainty in the theory of hemodynamics. The amount of work need to displace the blood in the systemic circulation, exceeds the work done by the left ventricle. With this, blood recovers increased flow resistance between the heartbeats with the Womersley number alterations in the rhythm of the accompanying electrocardiogram (ECG). Viscoelastic transformation is heavily expressed in coagulation. There must be a relationship between the ECG and blood transient flow resistance. The influence of the electromagnetic field on blood coagulation was studied. Venous blood was affected by the oscillated electromagnetic field (500 -5000 Hz), with the square wave input signal in 25 healthy individuals (15 males, 10 females in the age 18 -57 years). Electromagnetic irradiation (EMI) time of the sample 3 -10 min. Hypocoagulation in normal blood samples was revealed (decreased quantity of Platelets up to 10 -23 × 10 9 /L, Prothrombin index up to 9% -10%, Fibrinogen concentration up to 0.20 -0.21 g/L) and thrombolysis after the blood stasis. Ac electric field from the myocardial depolarization initiates electroacoustic phenomena. An emerging repulsing electromagnetic force acts on the red blood cells (RBC) and in addition to the pulse pressure from the heart, promotes blood motion and viscoelastic changes. The alterations of the blood inertial and elasticity, in addition to hemodynamics, are facilitated by the magnetic features of the hemoglobin. The external electromagnetic signal can manage the blood coagulation process, including thrombolysis.
Blood flow acceleration increases from the left ventricular outflow tract, to the sinotubular junction and the ascending aorta, while it must be decreasing due to the flow turbulences in the Valsalva sinuses and increased diameter of the vessel. Total energy of the pulse wave in the arterioles is up to 7.2 times higher, than in the ascending aorta, while it must be low due to the energy dissipation in the viscous flow, with the distance from the heart. Purpose of the study is identifying the additional possible energy source, for the arterial blood flow.Methods and materials: 12 healthy volunteer students (male) underwent echocardiography, ECG gated MRI of the heart for the visualization intracavitary flow in the ventricles, MR Angiography of the aorta. Blood flow velocities and acceleration were studied in the different sites of the heart and the aorta. Results: With the DU in the left ventricular outflow tract blood acceleration is 1430 ± 120 cm/sec 2 , in the sinotubular junction and ascending aorta 2395 ± 195cm/sec 2 , at the aortic arch 1390 ± 225cm/sec 2 , isthmus of aorta 2180 ± 135cm/sec 2 , middle thoracic aorta1260 ± 140m/sec 2 . With the MRI (TrueFisp. Mean curve), blood acceleration from the left ventricular outflow tract to the sinotubular junction is 3.5 ± 0.3 times higher and to the ascending aorta 2.5 ± 0.2 times higher. Systolic blood pressure from the ascending aorta to the femoral and saphenous elastic arteries enhancing 1.3 ± 0.1 times, increasing energy transmitted to the blood. Direction of the electric charge in the heart's ventricles from the circulating erythrocytes and in the fibers of the Purkinje (ECG), mathematically are coincident.Conclusion: Availability of the heart, as the possible single tool for the blood flow, looks imperfect. Electric oscillate field from the heart dipoles can be impact to the erythrocytes, forming the modulated naturally ultrasound vibration and associated with it colloid vibration current propagating distally to the all cell membranes. Blood motion in the heart chambers and arteries has the additional basis, besides the heart contraction: rotating blood particles in the heart chambers and in the arterial branching sites, with the concomitant oscillating electric field triggered from the heart, forms additional electromagnetic repulsing force for the charged particles, providing to the flow. Modulating ac electric field, transmitting by the oscillate blood particles, besides the flow, creates additional energy/signal source, enabling the spontaneous chemical reactions proceed across the cell membranes.
The objectives: Study the blood flow in aorta with the MRI and CT and express initial factors of atherosclerosis.Methods: Peak velocity, net flow and flow acceleration has been investigated at different sites of aorta in 17 healthy volunteers (18-52y). Blood radiodensity (HU) was measured by the CT scanner.Results: Blood flow acceleration in initial diastole, at the outer wall of isthmus, is 11.6 ± 0.6 times higher than that in systole. Net flow from systole to diastole increases 2.5 ± 0.5 times. At the outer curvature of isthmus, from the end of the systole to the initial of diastole, frequency of flow oscillation increases from 0.8Hz to 1.6Hz. Flow separation is more expressed here. Blood density (in HU) in the ascending aorta is 57.3 ± 3.5, at the terminal site of thoracic aorta 25.7 ± 3.1. Conclusion:At the outer wall of aortic isthmus, pulse pressure after the reflection is in resonance with the end systolic pressure drop. Amplitude of stress and frequency of oscillation in the boundary layer increases. Flow separates. Frequency dispersion destroys the flow cell aggregates, increasing blood entropy, whereas at the vessel wall, denudates endothelial sheet.
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