[Conformational states of NADH molecules in hydrated shell under weak electromagnetic irradiation].

The work deals with spectra of capillary waves of water distillate and water solution of NADH and dynamics of NADH under electromagnetic irradiation in the range of millimeters at different space frequencies of surface wave k.

[Effect of quercetin on proteasome activity in the aorta and heart tissues of spontaneously hypertensive rats].

To determine the role of proteasome proteolysis in the pathogenesis of hypertension, we have studied the proteolytic activity of the proteasome in the aorta and heart tissues of rats with spontaneous hypertension (line SHR), and used quercetin, the drug that can inhibit the activity of this multicatalytic complex. In the aorta of SHR, the activities of the proteasome were not significantly different from that observed in Wistar rats. At the same time, in the heart tissues the trypsin-like (at 40%, P > 0.05), and chymotrypsin-like (by 1.7 times, P < 0.03) activities were significantly less in SHR. Significant morphological changes (fibrosis of the left ventricle was 4.7%, aorta intima width was increased and heart weight index was higher by 21.6% (3.7 +/- 0.6 mg/g) compared with Wistar rats (2.9 +/- 0,4 mg/g, P < 0.004) were observed in these animals functional disorders (reduced stroke volume by 3 times (P < 0.0001), ejection fraction by 2.5 times (P < 0.0001), increased end diastolic pressure by 6.5 times (P < 0.005), end systolic pressure by 15% (P < 0.004)) were revealed. Pharmacological drug "Qvercetin" effectively inhibited trypsin-like and chymotrypsin-like proteasome activities in the aorta (2.7-fold (P < 0.005) and 2-fold (P < 0.003), correspondingly) and trypsin-like, and peptidyl-glutamyl peptide-hydrolyzing-like activities (2.4-fold, P > 0.05 and 9.3-fold, P < 0.02, correspondingly) activities in the heart, leading to a significant improvement of morphological and functional parameters of the heart. Whereas the drug "Qvercetin" that is widely used in clinical practice (especially in therapy of acute myocardial infarction) it could be recommended for the use in prevention of cardiac remodeling with high level of blood pressure.

[Correction of cardiodynamic disorders in experimental diabetes by omega-3 polyunsaturated fatty acids].

In experiments on rat hearts in vivo with the system for pressure-volume registration "Millar Instruments" cardiodynamic disorders were studied in experimental diabetes for their correction with omega-3 polyunsaturated fatty acids (PUFAs). The application of omega-3 PUFAs in animals with diabetes may improve cardiodynamic parameters--pump and diastolic function.

[Cardiohemodynamics and efficiency Frank-Starling mechanism in spontaneously hypertensive rats].

We studied cardiohemodynamics and efficiency Frank-Starling mechanism in 6-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar rats, using pressure-volume (PV) conductance catheter system (Millar Instruments, Houston, TX) to evaluate systolic and diastolic function in vivo. Rats were anesthetized with urethane. Cardiohemodynamics analyzed using PVAN 3.6 (Millar Instruments). We found that systolic and diastolic function of the heart in spontaneously hypertensive rats were lower, than in controls. We have shown, inhibition of the efficiency Frank-Starling mechanism, increasing arterial stiffness in spontaneously hypertensive rats. It's shown, less efficiency heart work, with more energy and more oxygen consumption in spontaneously hypertensive rats, may be associated with increasing arterial stiffness and decrease functional reserve of the heart.

[Interrelation between cardiac pump function disturbances and cardiac contractility after beta-adrenergic hyperstimulation of the heart in rats].

The complex of structural and functional changes of myocardium was investigated in experiments with rats with chronic beta-adrenergic activation for 1 month. We observed substantial attenuation of myocardial pump function, particularly reduction of stroke volume by 38.50% (P < 0.01), cardiac output by 42.38% (P < 0.01), and ejection fraction by 35.61% (P < 0.01). Furthermore, 2-fold increase of end-diastolic left ventricular pressure (P < 0.01) and rise of active relaxation constant Tau by 12.91% (P < 0.05) were observed. This indicates on an impaired diastolic function of the heart that is associated with accumulation of connective tissue elements in myocardium and increase of its end-diastolic stiffness that finally leads to cardiac pump function disturbances. Surprisingly, myocardial contractility was considerably augmented not only after the treatment with beta-adrenergic agonist but also on the 26th day after drug cessation. This phenomenon is associated with elevation of dP/dt(max) by 49.9% (P < 0.01), 2.5-fold increase of end-systolic elastance (P < 0.01) as well as maximal myocardial elastance by 42.53% (P < 0.05). It can be explained by compensatory influence of increased contractility that nevertheless failed to maintain adequate cardiac pump function and furthermore it may result in depletion of cardiac energy resource.