[Increase in nitric oxide generation in animal tissues during adaptation to short-term stressor exposure (EPR study)].
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Adaptation, Physiological↗
Biomedical subjects
A V Lapshin
Publications and source records attributed to A V Lapshin.
[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↗
[The intensification of nitric oxide synthesis in the aortic wall in experimental myocardial infarct].
The effect of experimental myocardial infarction on endothelium-dependent relaxation of isolated rat aorta and generation of nitric oxide in the aortic wall was studied. Three hours following myocardial infarction, the endothelium-dependent relaxation induced with acetylcholine was increased to 61 +/- 2% as compared with 41 +/- 4% in control (r < 0.05). The nitric oxide generation (EPR-assay) was 2.5 times increased in the aortic wall of animals subjected to myocardial infarction as compared with the control. The activated generation of nitric oxide may be provoked by the reduced minute volume of the heart and concomitant transient hypovolemia.
Acetylcholine↗
[Adaptation to short stress exposures prevents the enhancement of the endothelium-dependent reactions of the aorta in myocardial infarct].
Acute stress concomitant to the experimental myocardial infarction resulted in endothelial hyperactivation in the rat aorta as manifested in an increased inhibition of norepinephrine-induced contractions of smooth muscle, enhanced endothelium-dependent relaxation and a respective drop of the blood pressure. Preliminary adaptation of rats to short-term non-damaging stress exposure to a considerable extent prevented the stress-induced hyperactivation of endothelium and improved the postinfarction time course of the blood pressure.
Adaptation, Physiological↗
[The prevention of a postinfarct fall in pressure and hyperactivation of the aortic endothelium in the rat by using the antioxidant ionol].
The stress concomitant with experimental myocardial infarction resulted in endothelial hyperactivation of the isolated rat aorta. The hyperactivation was manifested in potentiated inhibition of norepinephrine-induced contractions of vascular smooth muscle, increased endothelium-dependent relaxation and respective drop of systemic blood pressure. Preliminary treatment of animals with synthetic antioxidant ionol prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure. The data suggest that the endothelial hyperactivation observed in acute myocardial infarction is induced by stress-induced activation of free-radical oxidation which results in a hyperproduction of endothelium-derived relaxing factor (nitric oxide).
Animals↗
Adaptation to short-term stress prevents post-infarction hyperactivation of the endothelium and decrease in blood pressure in rats.
The aim of the study was to elucidate the possibility of preventing the decrease in blood pressure (BP) and the endothelial hyperactivation that are induced by experimental myocardial infarction in rats. The endothelial hyperactivation manifested itself in potentiated endothelium-dependent relaxation and in attenuated contractile responses to noradrenaline in isolated rat aortas. Furthermore, the postinfarction changes in BP showed a negative correlation with the endothelium-dependent relaxation. Preliminary adaptation of rats to short-term nondamaging stress exposures or pretreatment with the antioxidant, ionol, prevented to a great extent both the postinfarction decrease in BP and the disturbances in endothelium-mediated responses of smooth muscle. Since, according to the literature, infarction-concomitant stress strongly activates free-radical processes which may result in a hyperproduction of endothelium-derived relaxing factor, it is suggested that the increased potency of anti-oxidant systems is the mechanism common to the protective effects both of adaptation and of ionol.
Acetylcholine↗
[The effect of experimental infarct and emotional-pain stress on the endothelium-dependent reactions of the isolated rat aorta].
Emotional-nociceptive stress, stress induced with a myocardial infarction, and stress following sham operation increased the effect of endothelium on the force and velocity of the smooth muscle contraction. Within 2 hrs after stress and 3 hrs after the coronary artery ligation, a considerable drop occurred in the rat arterial pressure followed by a facilitation of the aorta endothelium-dependent relaxation. Both these parameters were restored to the control level within 24 hrs. The facilitation of the endothelium-dependent relaxation of vascular wall seems to play a role in the drop of the vessels tone, in decrease of arterial pressure and, finally, in development of the cardiogenic shock in myocardial infarction in humans.
Acetylcholine↗
[Correlations between the endothelium-dependent relaxation of the aorta and arterial pressure in rats with myocardial infarction].
The effect of experimental myocardial infarction on endothelium-dependent relaxation was studied on isolated rat aorta and compared with the dynamics of arterial pressure (AP). It was shown that the endothelium-dependent relaxation of aorta was increased 1.8 times 3 h following the myocardial infarction. Simultaneously the drop in AP which had begun immediately following the experimental infarction became maximal. In 24 h both the indices were restored practically to the initial level. There was a significant negative correlation between the extent of endothelium-dependent relaxation and AP. It was suggested that the increase in endothelium-dependent relaxation could influence vascular tone, the drop in AP, and, finally, the development of cardiogenic shock in myocardial infarction in man.
Animals↗
[Effect of adaptation to periodic hypoxia on post-infarction fall of blood pressure and hyperactivation of the endothelium].
Acute stress concomitant to the experimental myocardial infarction has induced endothelial hyperactivation of the rat aorta exhibited in an increase of inhibition of norepinephrine-induced contractions of vascular smooth muscle, enhanced endothelium-dependent relaxation correlating with a fall of systemic blood pressure. Preliminary adaptation of rats to intermittent hypobaric hypoxia greatly prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure.
Adaptation, Physiological↗