Reactive hyperemia (RH) was produced after short-term (5-30 s) cessation of blood flow in experiments on anesthetized dogs following catheterization of the circumflex branch of the left coronary artery (with the chest intact) autoperfused with blood from the subclavian artery. The increase of the coronary blood flow observed after occlusion was shown to depend strictly on its duration. Deendothelization of coronary vessels decreased the RH significantly. In coronary bed the infusion of L-arginine was accompanied by an increase of RH and endothelium-dependent acetylcholine-induced vasodilation. L-arginine produced its effect only when the endothelium was intact, whereas NO synthase inhibition substantially decreased the RH and vasodilating response to intracoronary administration of acetylcholine. It was concluded that the RH was endothelium-dependent and that nitric oxide of endothelial origin was the active humoral component of this reaction.

Amino Acid Oxidoreductases↗

PubMedDate not supplied

[Endothelium-dependent vascular response in rabbits during prolonged experimental hypercholesterolemia].

It was shown in experiments on anesthetized rabbits that disturbances in endothelium-dependent relaxant (Ach-induced) and constrictor (hypoxia-induced) vascular responses depended on duration of high hypercholesterol diet and on the structural damage of the vascular wall as well as on changes in the functional activity of endotheliocytes. Short (1 month) hypercholesterolemia led to thickening of the blood-cellular barrier and promoted a decrease in the endothelium-dependent relaxant response to Ach. At the same time short hypercholesterolemia enhanced a constrictor component of the vascular smooth muscle (VSM) response to hypoxia. It may be explained by a different degree in disturbance of synthesis and/or release of the endothelial relaxing and constrictor factors. At the later period of hypercholesterolemia (2-9 month) parallel with a pronounced damage of the endothelium and development of atheromatous plaques, the impairment of the endothelium-dependent vascular responses became more and more pronounced. As a rule, Ach-induced relaxation in VSM was registered in sole experiments only and very often was either absent or transformed to contraction. Constrictor components of vascular response to hypoxia were significantly decreased as well. The above-mentioned disbalance between endothelial relaxant and constrictor factors in combination with structural damage of the endothelium and difficulty in transendothelial transport of these factors to effector elements of the vascular wall may cause vasospastic reactions in VSM at atherosclerosis.

Acetylcholine↗

PubMedDate not supplied

[The role of the thrombocyte-activating factor in inhibiting Na+,K(+)-ATPase in different tissues after ischemia and reperfusion of the small intestine].

Activity of transport Na+, K(+)-ATP-ase has been studied both in the ischemia-affected proximal section of the small intestine and in tissues which did not endure ischemia (the brain, renal cortex and the distal part of the small intestine) in dynamics 5, 30 and 60 min, after reperfusion of the ischemized small intestine of rats. It is shown that after 30 min-long ischemia of the small intestine, the Na+, K(+)-ATP-ase activity is inhibited in all the tissues mentioned. Maximal inhibition of the enzyme activity after 30 min long reperfusion is 74, 34, 94 and 58% for the brain, renal cortex, proximal and distal sections of the small intestine, respectively. It has been found that the blood serum from ischemized rats also exerts an inhibitory effect on the enzyme activity. Application of inhibitor of the thrombocyte-activating factor (TAF) BN52021 has permitted demonstrating its role in the protecting effect under conditions of Na+, K(+)-ATP-ase inhibition in the post-Ischemic period and inhibitory effect of the blood serum from ischemized rats on the enzyme activity. A conclusion is made that the TAF participated in the inhibitory effect of Na+, K(+)-ATP-ase activity in different tissues after ischemia of the small intestine of rats.

Animals↗

PubMedDate not supplied

Role of eicosanoids in the postischemic shock development.

Using premedication with indomethacin and/or quercetin, the role of the eicosanoids as one of the main shock mediators has been demonstrated in anesthetized dogs using a model of postischemic shock. Hemodynamic disturbances were correlated with an increment in eicosanoids blood levels both in time and value courses. The results testify to the vascular endothelium injury in all investigated regions. This event might be a starting point of the disturbances in balance between a necessity and real flow in working organs under shock-like states. Therefore, a damage in endotheliocytes function is the first and may be a leading factor in the development of postischemic disturbances of circulation. Pretreatment with the inhibitors of eicosanoids biosynthesis prevented the reperfusion-evoked hemodynamic disturbances.

Animals↗

PubMedDate not supplied

[Effect of low doses of radiation on the contractility of vascular smooth muscle at stretch].

The contractile reactions of the vascular smooth muscles at their stretch were studied in the isolated strips of v. porta of control rats and those, which had been born and exposed for 6 months to low intensity small dose radiation (Experimental Base in Chernobyl). The results obtained revealed the "mosaic" and significant disturbances (60% of cases) of the muscle contractile activity in the experimental animals. The myogenic mechanisms, which provide for the length-force dependence of the vessel's smooth muscles, were less effective in experimental vs. control animals. A major reason for the above changes may be the disturbances of the endothelium's function.

Animals↗