The purpose of this study was to investigate the effects of prior dietary supplementation with creatine (Cr) or cyclocreatine (Cy, a synthetic analogue of Cr) on high energy phosphate metabolism of the ischemic myocardium. To this end, 48 rats were fed the following powdered rat chow diet for 21 days: 16 were fed chow without additives (CON); 16 were fed a diet containing 1 % Cr by weight (CR); 16 were fed a diet containing 1 % Cy by weight (CY). At the end of the feeding period, rats were anesthetized, hearts harvested and perfused in the Langendorff mode using Krebs-Henseleit buffer (maintained at 37 °C, equilibrated with 95% 02/5% CO2) to which 11 mM glucose was added. ³¹P nuclear magnetic resonance (NMR) studies of myocardial bioenergetics were done using a Bruker AM 500 spectrometer. After acquisition of preischemic spectra, global ischemia was produced by clamping aortic inflow. Ischemia was maintained until adenosine triphosphate (ATP) became NMR invisible (CON =34 ± llmin;CR = 32 ± 13min;CY = 56 ± 13min;p < 0.05 CY vs. CR and CON). Half-lives of ATP were 19 min for CON and CR and 37.5 min for CY; half-lives of phosphagen were 4 min for CON and CR and 11 min for CY. Time for return of mechanical function (heart rate × systolic pressure) after ischemia was similar for all three groups (CON = 28 ± 28, CR = 34 ± 22, and CY = 22 ± 15 min), even though the CY group was subjected to longer periods of ischemia). These data indicate that CY, but not CR, pretreatment provides myocardial protection either during and/or after ischemia and allows return of mechanical function after much longer episodes of ischemia than in CON and CR. One factor in the mechanism of protection may be the prolonged maintenance of phosphagen due to the higher equilibrium concentration of phosphocyclo-creatine which in turn provides substrate for continued synthesis of ATP during and after ischemia, thus defining Cy as a bioenergetic protective agent. Other mechanisms of protection remain to be defined.

Goal of research. Study the role of thrombosis risk factors and polymorphisms in genes in young age patients with acute coronary syndrome (ACS).Materials and methods. Te study included 299 patients of age 25 to 44 years old with ACS were treated from 2012 to 2017 at the department of myocardial infarction 1st KGBUZ Altay regional cardiological clinic. Te middle age of patients with ACS was 40.3 ± 0.2 years. Te control group included of 53 apparently healthy volunteers aged from 25 to 44 years old, the average age those patients was 39.94 ± 0.79 years. Also, those patients hadn’t any comorbid conditions. Te control group hadn’t any datas of ischemic heart disease by the results of exercise tolerance tests. All patients had standard clinical, anamnestic, biochemical tests, lipid profle, fasting plasma glucose, electrocardiogram, echocardiography and coronaroangiography, also they were determined growth and weight with body-weight index. 116 patients from the ACS group and 53 patients fromthe control group had screening of polymerase chain reaction for determine polymorphism of the FII genes G20210-A, FV G1691-A, and MTHFR C677-T.Results. We identifed the most signifcant sets of risk factors associated with ACS in young age patients based on our multifactorial statistical analysis with binary logistic regression. Tis combination of risk factors was: increased levels of low-density lipoproteins, decreased levels of high-density lipoproteins, smoking, existence of MTHFR homozygous polymorphism, heredity in combination with smoking, FV homozygote, MTHFR homozygote, smoking with MTHFR-homozygote.Conclusion. Te ability predicting the risk of developing cardiovascular disease in young people based on traditional risk factors, partly modifable, as well as the researching of "new" risk factors, opens up new opportunities for developing a clinical approach of treating young patients with high risk of ACS.

The effects of acute volume and/or pressure loading on myocardial metabolic and mechanical function were studied in 13 dogs. Volume loads were applied by shunting the abdominal aorta to the vena cava using polyethylene tubing (5 mm inner diameter). A plastic regulator allowed shunts to be opened or closed. Dogs were heparinized (100 units/kg) to prevent shunts from clotting. To study the effects of pressure loading, a norepinephrine infusion (1 µg/kg/min) was administered. Mechanical function of the heart was evaluated using heart rate × systolic blood pressure (HR × SBP), cardiac output (CO), pressure × volume work (systolic blood pressure × stroke volume); (P × V), and oxygen consumption (MVO₂) to estimate external myocardial work. Metabolic function was evaluated by ³¹P NMR. Phosphocreatine/adenosine triphosphate (PCr/ATP) ratios were used to estimate the bioenergetic regulation of oxidative phosphorylation during increased work load. HR × SBP, CO, P × V, and MVO₂ were correlated with PCr/ATP. Although there was some variability, generally volume loading was associated with an increase in HR × SBP, CO, P × V, and MVO₂ accompanied by no change, or small increases or small decreases in PCr/ATP throughout the loading period. These data indicate that the heart bioenergetics are quite stable during volume and/or pressure loading and that ³¹P spectroscopy methods can document this stability and tight metabolic regulation during in vivo loading conditions.