A controlled randomized investigation on the experimental model of contrast-agent (iopromide) induced nephropathy (ÑIN) in male rats showed that combined hydratation therapy with NAD + containing cytoprotective and anti-ischemic drug nadcin leads to decrease in the creatinine level and blood urea nitrogen (BUN) in plasma in 72 h after CIN reproduction. A linear positive strong correlation between endothelin (ET-1) level and O 2 generation (r = 0.78, p < 0.001) was observed, while no coupling was found between the production of hydrogen peroxide and ET-1 level (r = 0.13, NS), and also between the ET-1 level and catalase activity (r = 0.41, NS). In contrast to the hydration treatment, the inclusion of nadcin in therapy leads to normalization of the level of ET-1 and ET-1/creatinine ratio in blood, redox-potential NAD/NADH and NADP/NADPH in blood and kidney, inhibits the hyperproduction of free radicals, and activates the blood and renal antioxidant defense systems. Determination of the content of ET-1, ET-1/creatinine ratio, and redox-potential in plasma is recommended for use as early markers of a higher risk of renal dysfunction development during the administration of x-ray contrast agents.

The aims of study– a development of biochemical algorithms of early diagnostic of severity of CHF in patients with DM and IHD and analyze interrelationships between plasma redox-potential, as a marker of progressive of tissues metabolic remodeling and cardiac hypertrophy and markers of progressive of DM, neurohumoral markers of severity of CHF, and frequency of heart rhythm disturbances.Materials and methods.172 patients, male / female (45–65 years), with diagnosis of DM (metabolic decompensation of carbohydrate metabolism, HbА1c – 7.4 ± 1.9 %) during 3–15 years, accompanied with IHD and symptoms of CHF I–IV NYHA functional class (FC). The first point of investigation was examined markers of DM progression HbА1c, changes in FC of HCHF and evidenced prognostic neurohumoral markers of myocardial dysfunction NT-proBNP, and as a second (surrogate) point – changes in redox-potential NAD / NADH and total pool of pyridine nucleotides.Results.Mean NYHA FC CHF in cohort of DM patients and IHD was 2.4 ± 1.2, mean point of CHF estimated by scale of symptoms of CHF was 6.7 ± 0.6, mean distance in 6-minute test was 212 ± 26 m, concentration of neurohumoral markers of myocardial dysfunction NT-proBNP 178 ± 26 fmol / l at the level of HbA1c = 7.8 ± 1.0 %, mean redox-potential of plasma, НАД / НАДН, 0.71 ± 0.06 and total pool of pyridine nucleotide 15.1 ± 1.2 μmol / mg protein of plasma. For the first time was shown that changes in redox-potential and sum of pyridine nucleotide coupled with severity of CHF (FC of CHF), eliminated the correlation between NAD / NADH and HbA1c (r = –0.79, p<0.001), and NTproBNP (r = –0.73; р <0.001), and increasing of tumor necrosis factor alpha (TNF-α, r = –0.73; р <0.001). Simultaneously maintenance decreasing of NAD / NADH and sum of pyridine nucleotide in plasma of patients with DM and IHD coupled with increasing of daily mean values of paired supraventricular and ventricular extrasystoles.Conclusions.In patients with DM and CHF with left ventricular dysfunction the decreasing of redox-potential level in plasma could be recommended as a markers of increasing of metabolic remodeling and progression of cardiac hypertrophy.