Modulation of hydrogen sulfide synthesis improves heart function and endothelium-dependent vasorelaxation in diabetes.

Diabetes dramatically increases the risk of cardiovascular complications. The endothelial dysfunction and diastolic heart dysfunction are associated with a decreasing level of hydrogen sulfide (HS) and inhibition of the activity of endothelial nitric oxide synthase (NOS) in diabetes. The aim of this study is to investigate the effect of modulation of HS synthesis on heart functions and vasorelaxation in diabetes.

H S donor improves heart function and vascular relaxation in diabetes.

Background And Aims: Diabetes dramatically increases the risk of cardiovascular complications and mortality. Hydrogen sulphide plays an important role in reducing oxidative stress. Several studies demonstrated that hydrogen sulphide protects islet beta cells from oxidant stress damage and decreases apoptosis.

The role of hydrogen sulfide in diastolic function restoration during aging.

The objective of the study was to examine the effect of exogenous hydrogen sulde donor; sodium hydrosulfide (NaHS), on thefree radical generation, cNOS uncoupling in the myocardium, and diastolicfunction in old rats. To evaluate diastolic function of the heart, we used pressure-volume (PV) conductance catheter system (Millar Instruments, USA). It was shown that H2S levels in.

[EFFECT OF PROPARGYLGLYCINE UPON CARDIOHEMODYNAMICS IN OLD RATS].

Aging increases the risk of cardiovascular diseases. The objective of this study was to show the effect of propargylg- lycine (PPG) upon cardiohemodynamics in old rats. We used pressure-volume (PV) conductance catheter system (Millar Instruments, USA) in order to evaluate systolic and diastolic function in vivo.

[PHYSICAL EXERCISE TRAINING CAN- CELS CONSTITUTIVE NOS UNCOUPLING AND INDUCED VIOLATIONS OF CARDIAC HEMODYNAMICS IN HYPERTENSION (PART III)].

In the heart and heart mitochondria spontaneously hypertensive rats investigated the effect of physical exercise training (swimming in a moderate and excessive training mode) on the physiological indicators of cardiac hemodynamics and biochemical parameters that characterize the level of oxidative and nitrosative stress. The index of coupling Ca(2+)-dependent constitutive NO-synthases (cNOS = eNOS + nNOS) and biochemical index of dysfunction were calculated. It turned out that both modes of training is completely restored, and even exceed the reference values in untrained rats Wistar conjugate cNOS state and Ca(2+)-dependent synthesis of nitric oxide (NO).

[ENDOTHELIAL MONOCYTEACTIVATING FACTOR II CANCELS OXIDATIVE STRESS, CONSTITUTIVE NOS UNCOUPLING AND INDUCED VIOLATIONS OF CARDIAC HEMODYNAMICS IN HYPERTENSION (PART II)].

The purpose of this study was to investigate the effect of EMAP II on free radical state of the heart and blood vessels, to restore cNOS coupling and cardiac hemodynamics in spontaneously hypertensive rats. It was found that, due to the combined inhibition of oxidative and nitrosative stress, EMAP I quickly restores impaired in hypertension constitutive de novo synthesis of NO by restoring cNOS coupling. Restoration by EMAP II of constitutive de novo synthesis NO abolished cardiac and endothelial dysfunction in spontaneously hypertensive rats.

[NOS UNCOUPLING IS ACCOMPANIED WITH INDUCTION OF THE OXIDATIVE STRESS AND THE CARDIOHEMODYNAMICS DISTURBANCES IN HYPERTENSION].

We compared the performance of cardiaohemodynamics and indicators of oxidative and nitrosative stress in the heart and aorta in normotensive Wistar rats (WKR) and spontaneously hypertensive rats (SHR). On the basis of experimentally determined parameters to calculate cNOS uncoupling index and biochemical index of function (BIF) in these organs of the cardiovascular system. In the heart, and especially in the aorta of SHR develop a combined oxidative and nitrosative stress that leads to cNOS uncoupling, BIF lowering that correlate with lowering of systolic and diastolic functions, inhibition of the efficiency Frank-Starling mechanism, oxygen consumption of the heart and increasing arterial stiffness.