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Background and Aims It is traditionally believed that high consumption of sodium chloride leads to the development of arterial hypertension, which, in turn, will cause heart remodeling. However, more and more evidence is accumulating that a high sodium chloride content in the diet can cause heart damage without increasing blood pressure (BP). This is confirmed in experiments on rats. In addition, in animals of this species, supplementing a high-salt diet with soy proteins can prevent cardiovascular damage. Whether such mechanisms operate in primates remains unclear. Method The study was performed on male Macacus fascicularis. Monkeys were included in the experiment at the age of 4.6 -7.0 years and had a body weight of 5,5-7,5kg. Animals were divided into 3 groups. The first (control) included 5 animals, received standard ration; the second – 5 animals, received diet with high sodium chloride content (8 g NaCl/1 kg of the feed); the third – 6 animals, who were on a diet with high salt contents supplemented by soya isolated proteins (200 g/kg of the feed). In anesthetized animals measured blood pressure and performed an echocardiographic investigation. Follow up period lasted four month. Results Initially, in all groups of animals, blood pressure levels (Mean(SEM)) and echocardiographic parameters did not significantly differ. During the observation period, the studied parameters did not change much. For example, in the first group, an ejection fraction (EF) increased from 61.7(1.67) to 71.6(4.74), %; P=0.045. In the same group, a tendency toward a decrease in the left ventricle end-systolic dimension (1.50(0.056)vs 1.29(0.118), mm; P=0.079) was noted. Whereas the level of systolic and diastolic blood pressures in this group (for example, systolic BP: 115.4(3.95)vs 126.0(5.39), mm Hg; P=0.134) as well as in other groups of monkeys did not change significantly. Nevertheless, after four months of observation, the level of systolic blood pressure in the second group (126.0(5.39) mm Hg) of animals was significantly higher than in the first (103.0(5.54), P=0.0118) and nonsignificantly - in the third (104.0(8.39), mm Hg; P=0.065). EF in the end of follow up period in second group (71.6(4.74%) was significantly higher than in control (58.1(2.72),%; P=0.039) but not in the third group (60.9(5.03),%; P=0.162). Tricuspid annular plane systolic excursion in second group (1.02(0.08), mm) had an insignificant tendency to increase in comparison to the first (0.782(0.096), mm; P=0.094) or third (0.818(0.049), mm; P=0.052) groups. Conclusion Our data do not exclude the possibility that a high salt content in the food of lower primates can contribute to an increase in blood pressure and a change in heart function. However, to resolve the issues of the relationship between changes in heart function and the level of blood pressure and the presence of the cardioprotective effect of soy proteins under these conditions, longer observations are needed.

Background. Even a moderate decrease in glomerular filtration rate leads to an increased risk of cardiovascular diseases (CVD), which is the leading cause of mortality in patients with chronic kidney disease (CKD). Left ventricular hypertrophy (LVH) underlies CVD development in renal dysfunction. The prevalence of LVH in patients with CKD stages 2–4 is 50–70 % and reaches 95 % at the beginning of dialysis, which significantly exceeds the number of cases in general population (15–21 %). Common hemodynamic factors associated with chronic kidney damage —hypertension (HTN), activation of the renin-angiotensin system, anemia, fluid and sodium retention, and others largely explain the high prevalence of LVH among patients with CKD. Nevertheless, the existence of additional non-hemodynamic mechanisms of myocardial remodeling (MR) is evident.Objective. To investigate the associations between the MR physiological/histological characteristics and laboratory parameters of calcium-phosphate metabolism in the initial stages of experimental CKD. Design and methods. Four groups of spontaneously hypertensive rats (SHR) were studied (n = 35): 3/4 nephrectomized rats (Nx) one month exposed after surgery (Nx(1), n = 9), 5/6 Nx two months after surgery (Nx(2), n = 8), sham operated rats one month after surgery (SO(1), n = 9) and two months after surgery (SO(2), n = 9). Myocardial mass index (MMI), systolic blood pressure (BP), proteinuria, creatinine (Cr) concentration, total calcium (Ca) and inorganic phosphate (Pi), 25-OH vitamin D (25OHD) and parathyroid hormone (PTH) in serum, myocardial morphology were studied in all experimental animals.Results. The models corresponded to the 1–3 stages CKD. There were no significant changes in serum total Ca (p = 0,066), Pi (p = 0,051) and PTH (p = 0,015) concentrations, the level of 25OHD was significantly lower in Nx(2) rats vs control (p = 0,015). MMI increased in all nephrectomized rats (p = 0,008). The cardiomyocytes (CM) thickness increased in Nx(1) and Nx(2) animals compared to the corresponding controls (p = 0,010, p = 0,002). A significant increase in interstitial (IF) and perivascular (PF) fibrosis occurred in Nx(2) rats with more damaging influence (p = 0,017, p = 0,004). CM thickness, IF and PF increased with the elevation of BP (r = 0,39, p = 0,038, r = 0,47, p = 0,026, r = 0,49, p = 0,031) and serum Cr (r = 0,68, p = 0,001, r = 0,61, p = 0,003, r = 0,69, p = 0,001), and the decrease in serum 25OHD concentration (r = –0,045, p = 0,047, r = –0,50, p = 0,020, r = –0,52, p = 0,012). Multiple linear regression analysis showed, that 25OHD is an independent predictor of myocardial fibrosis (IF: β = –0,38 ± 0,18, p = 0,047, PF: β = –0,34 ± 0,15, p = 0,032).Conclusions. The initial stages of CKD accompanied with HTN are associated with serum 25OHD concentration decrease CM hypertrophy and myocardial fibrosis. The CM growth is an earlier event in relation to the interstitial fibrosis. The obtained data suggest a possible role of vitamin D deficiency in the development of myocardial fibrotic lesions.

620.191.001.57(045) and A. V. Bashta A simulation model for multiple fracture has been developed that reproduces random processes of initiation, growth, and coalescence of dispersed surface cracks. The model is based on the method of statistical simulation (Monte Carlo method) and on the fracture regularities determined experimentally. The main factor responsible for fracture is found to be the coalescence of dispersed cracks, especially at the final stage, which accounts for about 30% of the total life. The ultimate state of a structure is defined by the condition according to which the length of the largest of the available damages is bigger than the calculated value of the maximum crack length.Introduction. The presence of a large number of short cracks scattered over a limited surface area is one of the manifestations of damages in machine parts under cyclic loading. Fracture of materials induced by the processes of initiation, growth, and coalescence of cracks, which are continuous in time, is universal [1], it is called multiple (dispersed or multisite) and is characteristic of many damaging factors, e.g., isothermal and nonisothermal fatigue [2][3][4][5], cyclic creep [6], and corrosion [7].Multiple fracture (MF) is of stochastic nature due to a random process of crack initiation in time, as well as random character of their dispersion on the surface, the rate of their growth and coalescence. During the coalescence of dispersed short cracks, their dimensions increase in a jump-like manner. Under condition of high concentration of defects, this may lead to an unexpected initiation of a critical (inadmissible in size) crack.The amount of experimental data on multiple fracture is rather limited. This is explained by the laboriousness of identification and complexity of monitoring the behavior of a large number of small-size defects on the specimen surface. Yet, the available experimental data make it possible to reveal general manifestation of the multiple fracture and, on this basis, to construct a mathematical model for the process and obtain the required results by means of a numerical experiment. The objective of this work was to develop a simulation model for multiple fracture.The model presented here simulates the processes of random initiation, propagation, and coalescence of surface microcracks occurring simultaneously. The damage evolution is described with allowance for the force interaction of the cracks in close proximity during their coalescence.The ultimate state is characterized by the appearance of a crack of a given critical size or by the formation of a cluster, which penetrates the damaged surface, due to large-scale coalescence of cracks of high concentration.The model is based on the method of statistical simulation (Monte Carlo method). This approach found application in the investigations of multiple surface cracking of materials [5,7,8] and each model is based on individual initial prerequisites depending on the problem to be solved.Initial Prerequisites of the Model. The initial p...