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S Iu Mashina

Publications and source records attributed to S Iu Mashina.

12 recordsLinked to original sources
PubMed2001

[Correction of NO-dependent cardiovascular disorders by adaptation to hypoxia].

Spontaneously hypertensive rats (SHR-SP) were adapted to intermittent hypobaric hypoxia in an altitude chamber for 40 days. The adaptation to hypoxia prevented an excessive endothelium-dependent relaxation and hypotension characteristic of myocardial infarction. The adaptation also attenuated the increase in blood pressure and prevented impairment of the endothelium-dependent relaxation in SHR-SP. The universal nature of the adaptation allows to use it for correcting many cardiovascular disorders related to diverse alterations of NO metabolism.

Adaptation, Physiological↗
PubMed1993

[Decrease in constrictor response and increase in dilator response of the resistant artery in experimental myocardial infarction: effect of adaptation to hypoxia on this phenomenon].

After adaptation to hypoxia experimental myocardial infarction does not result in enhanced vasodilatory responses of isolated tail artery from rat to acetylcholine and isoproterenol. At the same time the vascular reactivity to norepinephrine and phenylephrine is enhanced. These data may explain the previously described improvement in postinfarction time course of the blood pressure due to preliminary adaptation to hypoxia.

Adaptation, Physiological↗
PubMed1993

[Adaptation to periodic hypoxia decreases vasoconstrictor and increases vasodilator responses of resistant arteries].

Adaptation to intermittent hypoxia resulted in reduced vasoconstrictor responses of rat tail artery elicited by sympathetic nerve stimulation due to desensitization of alpha- and activation beta 2-adrenoceptors. Endothelium-dependent relaxation was enhanced under the impact of adaptation to intermittent hypoxia. These shifts may play a part in antihypertensive effect of adaptation to hypoxia which has been proved earlier.

Acetylcholine↗
PubMed1993

[Effect of fish oil with a high content of polyunsaturated fatty acids (eiconole) on myogenic tone and magnitude of the constrictor and dilator responses in isolated tail artery of rats].

A long-term excess of polyunsaturated fatty acids in diet resulted in more than twofold reduced myogenic tone of isolated rat tail artery. Vasoconstrictory responses to norepinephrine and phenylephrine were reduced as well. At the same time the excess of dietary polyunsaturated fatty acids resulted in enhanced vasodilatory responses to isoproterenol and acetylcholine. This complex of universally targeted shifts may play a significant part in the antihypertensive effect of excessive polyunsaturated fatty acids in diet.

Acetylcholine↗
PubMed1993

[The effect of adaptation to a course of stress-inducing electrostimulation on the reactivity of an isolated resistive artery].

Repeated stress adaptation made with a course of electrostimulation was found to result in changes in the responsiveness of the rat isolated tail artery taken from adapted animals. These changes appeared as decreased vasoconstrictive responses to norepinephrine and significantly higher endothelium-dependent vasodilation induced by acetylcholine and the beta-agonist isoproterenol. The regulatory shift occurred towards vasodilation of the resistive artery makes the studies of the impact of stress adaptation on blood pressures in hypertension promising.

Adaptation, Physiological↗
PubMed1990

[The suppression of neurogenic vascular reactions by a factor released into the blood during immobilization stress].

In isolated segment of the rat tail artery perfused with the animal donor's blood the effect of suppression of neurogenic vascular tonus, in immobilization of the animal donor, was found in 80% of cases. In 62% of cases, the suppression occurred at the beginning of the immobilization and seemed to be due to the effect of hypothetical humoral factor on the synapse area. In 38% of cases, the suppression started within 30-40 min of the immobilization start and had a different cause. The adaptive significance of these responses is discussed.

Animals↗
PubMedDate not supplied

[The production and deposition of nitric oxide during adaptation to hypoxia].

It is common knowledge that adaptation to hypobaric hypoxia provides for a number of protective NO-dependent effects in the organism. However, many aspects of its influence on NO metabolism remain unclear. In this work we studied the relationship between NO production and deposition in the course of adaptation to hypoxia. No production was assayed by the total concentration of nitrates and nitrites in rat serum, while the volume of NO depot was determined from the level of isolated aorta relaxation in response to diethyldithiocarbamate in vitro. In the course of adaptation to hypoxia, nitrate and nitrite concentration increases as well as NO deposition in the vascular wall. The volume of NO depot correlated reliably with the serum concentration of nitrates and nitrites. Hence, adaptation to hypoxia increases NO production and deposition, which can underlie its NO-dependent protective effects.

Adaptation, Physiological↗
PubMedDate not supplied

[Prevention of nitric oxide hyperproduction by adaptation to stressor effects].

As was shown earlier, acute hypotensive shock induced by nitrogen oxide (NO) hyperproduction can be prevented by dosed adaptation to environmental factors. In this work we tested the hypothesis that the mechanism of this adaptive effect is based on limiting NO hyperproduction. It was shown that rat adaptation to stress completely prevented arterial depression and sharply increased revival rate of the animals after heat shock. Hypotension induced by heat shock was accompanied by almost 2.5-fold increase in NO production (EPR analysis) as compared to the control. At the background of preadaptation, heat shock did not increase NO production relative to the animals not subjected to heat shock. The data obtained agree with the proposal that the adaptation initiates NO-dependent mechanisms of limiting NO hyperproduction. Such limiting seems to be negatively regulated by NO.

Adaptation, Physiological↗