[Role of endothelial glycocalyx in mechanogenic control of arterial hydraulic resistance].

The review was focused on the data demonstrating that flow induced arterial dilation depends not only on intact endothelium but on intact endothelial glycocalyx, as well. These data demonstrate that filaments of the endothelial glycocalyx serve as mechanotrasducers since their shear stress induced deformations stimulate endothelial cells to release nitric oxide.

[Role of cooperation of myogenic response and sensitiveness of endothelia to shear stress of change inadjusting of organ blood stream].

In the review we analyze a counteraction of two mechanogenic mechanisms that control vascular hydraulic resistance: 1) myogenic response, and 2) ability of vascular endothelium to change the smooth muscle tone in responce to changes of wall shear stress. We showed that this counteraction provides an adequate blood supple of organs, autoregulation of organ blood flow and stability of the vascular system.

[Effect of malondialdehyde on deformability of human umbilical vein endothelial cells].

In experiments on cultured endothelial cells of human umbilical vein, we found that incubation of these cells during 24 hours with malondiaidehyde (cone. 200 microM) led to over two-fold increase in the cell stiffness. These data suggest that manifold augmentation of malondialdehyde concentration during oxidative stress may be accompanied by a considerable weakening of endothelium-dependent shear stress-induced arterial dilation.

[Role of mechanosensitivity of the endothelium in weakening of the vascular bed vasoconstriction]. / Rol' mekhanochuvstvitel'nosti éndoteliia v oslablenii konstriktornykh reaktsii sosudistogo éndoteliia.

The effect of control of arterial diameter by the shear stress at the endothelium on noradrenaline-induced constriction of femoral vascular bed was investigated in anaesthetised cats. We compared noradrenaline-induced responses during the perfusion of the hindlimb at a constant blood flow and at a constant pressure as vasoconstriction is accompanied by an increase in wall shear stress only in the former case. We found that the same concentration of noradrenaline at a constant flow caused an augmentation of vascular resistance that was considerably smaller than at a constant pressure perfusion. This difference was almost eliminated after either removal of the endothelium or selective impairment of the endothelial sensitivity to the shear stress. These findings demonstrate that the control of arterial smooth muscle tone at a constant blood flow by shear stress at the endothelium does weaken noradrenaline-induced vasoconstriction.

[Using hydraulic input impedance in determination of changes in the arteries of different calibre]. / Ispol'zovanie metoda vkhodnogo gidravlicheskogo impedansa dlia opredeleniia izmenenii sostoianiia arterii raznogo kalibra.

In anaesthetised cats, the arterial input impedance in combination with seven-element lumped-parameter model was used to estimate the resistance change in arteries of different caliber. The results show that the method gives reasonable estimations of changes in hydraulic resistance of arterial vessels of different caliber. We found that the method of vascular input impedance permits to reveal and assess quantitatively local constrictions and dilations as well as hemodynamically insignificant stenosis of conduit arteries.

[Input impedance for studying hydraulic parameters of the vessel system]. / Vozmozhnost' ispol'zovaniia metoda vkhodnogo impedansa dlia opredeleniia gidravlicheskikh parametrov sosudistoi seti.

Vascular input impedance can be used as an effective tool in estimating hydraulic parameters of arterial bed. These parameters may be interpreted as hydraulic resistance, elastance and inertance of particular sites of the arterial system. There is no significant difference between these parameters and those obtained through a direct measurement.

[The role of deformability of endothelial cells in the arterial response to shear tension]. / Rol' deformiruemosti éndotelial'nykh kletok v reaktsiiakh arterii na izmeneniia napriazheniia sdviga.

Treatment of the femoral artery luminal surface with glutaraldehyde dimere or dithiosuccinimidyl propionate reduced or eliminated flow-induced dilation, the responses to acetylcholine and the ATP being preserved. The findings suggest that the endothelial cells perceive changes in shear stress and that the cell stiffness is a factor subject to the influence of the magnitude of flow-induced arterial dilation.

[The role of endothelial mechanosensitivity in vessel bed responses to changes in blood pressure in cats]. / Rol' mekhanochuvstvitel'nosi éndoteliia v reaktsiiakh sosudistogo rusla na izmeneniia davleniia u koshek.

In 19 anaesthetised cats, the response of vascular bed to increasing perfusion pressure at a constant blood flow perfusion consisted of two phases: a myogenic constriction and a subsequent arterial dilatation. The latter depended on ability of the endothelium to relax the smooth muscle under stress. The findings suggest that the control of the smooth muscle tone by a stress has to fight against the myogenic constriction and thus determines the changes in vascular resistance induced by an increased arterial pressure.

[The anticonstrictor effect of endothelial sensitivity to shear stress]. / Antikonstriktornyi éffekt chuvstvitel'nosti énodeliia k napriazheniiu sdviga.

Responses of the femoral artery to drops in transmural pressure and to norepinephrine revealed the anticonstrictor effect of the endothelium sensitivity upon a stress action. The effect was less obvious at high flow rate. The data obtained suggests that the endothelium sensitivity to stress inhibits the arterial constrictor responses irrespective of the nature of the constrictor stimuli.

[The regulation of the lumen of the major arteries in accordance with the shear stress on the endothelium]. / Reguliatsiia prosveta magistral'nykh arterii v sootvetstvii s napriazheniem sdviga na éndotelii.

A decrease in the blood viscosity due to hemoconcentration, caused arterial dilatation. These viscosity-induced responses depended on intact endothelium. The dilatory responses caused by equal increments in flow rate, increased in systemic hemoconcentration and decreased in systemic hemodilution. The data obtained corroborate the suggestion that stress applied to endothelium is the key signal in the control of arterial lumen by the blood flow rate.

[Nitrogen oxide is not an agent of endothelium-mediated arterial dilatation to an increase in the blood flow rate]. / Oksid azota ne iavliaetsia mediatorom oposreduemoi éndoteliem dilatatsii arterii na povyshenie skorosti krovotoka.

I. v. administration of inhibitors of endothelium-mediated synthesis of the oxide of nitrogen raised the arterial blood pressure, constricted the femoral artery and decreased the acetylcholine- and ATP-induced vaso-dilatation in anesthetized cats. However, the dilatation induced by an increased blood flow velocity, was not affected. The data obtained suggest that the endothelium-dependent arterial dilatation is not mediated by oxide of nitrogen formed from L-arginine.

[Selective glutaraldehyde blockade of the sensitivity of arteries to blood flow velocity]. / Izbiratel'noe vykliuchenie chuvstvitel'nosti arterii k skorosti krovotoka glutarovym al'degidom.

The possibility of selective blockade of arterial sensitivity to flow rate was investigated. The method under study was based on the ability of glutaraldehyde to increase cellular rigidity. As flow-induced arterial dilatation depends on endothelial sensitivity to force, the increased rigidity of endothelial cells leads to the reduction of the dilator stimulus. It was shown that the treatment of endothelium with dimerized glutaraldehyde (0.01-0.03%, 30 sec) removed flow-induced arterial dilatation, without abolishing acetylcholine-evoked dilatation.

[Blood flow velocity--a constantly acting factor in dilatation of the large arteries]. / Skorost' krovotoka--postoianno deistvuiushchii faktor dilatatsii krupnykh arterii.

Acute experiments on cats have demonstrated the presence of renal artery sensitivity to the bloodstream velocity; the artery is enlarged with the blood flow increase and is narrowed with its decrease. The dilatation of the artery caused by the double increase of the blood flow (from 20 to 40 ml/min) is 23 +/- 8%. It has been established experimentally that carotid, femoral and renal arteries of cats respond to minor changes (of the order of 1 ml/min) in the volumetric velocity of the bloodstream by changing their diameters. Therefore, the arteries continuously follow the bloodstream velocity changes by changing their diameters. It may thus be concluded that the bloodstream itself is the artery dilatation factor.

[Changes in the carotid artery tonus of cats in response to changes in the blood flow rate]. / Izmeneniia tonusa sonnoi arterii koshek v otvet na izmeneniia skorosti krovotoka.

It was shown in acute experiments on cats that the carotid artery is sensitive to the rate of blood flow. The increased blood flow with the unchanged perfusion pressure causes carotid artery enlargement which is maintained throughout the entire period till the arterial blood flow remains increased. The reduction of blood flow to the initial level is accompanied by the diameter returning to the initial value. The latent period of the dilatatory response of the carotid artery to the increased blood flow does not exceed 25 s, the maximal magnitude of the response averages 25 +/- 6%. In the physiological blood flow range (from 10 to 50 ml/min) the response is linearly dependent on the degree of the blood flow increase.

[Automatic stabilization of the pressure in the large arteries during blood flow changes]. / Avtomaticheskaia stabilizatsiia davleniia v krupnykh arteriiakh pri izmeneniiakh krovotoka.

A method is proposed of automatic stabilization of per fusion pressure in the large arteries during changes in the flow velocity. The method is based on using in series with the artery a variable hydraulic resistance in value of which is changed in accordance with the blood flow rate in the artery. This provides pressure stabilization in the artery.

[Regulation of the femoral artery diameter during changes in the rate of flow of perfusion solutions]. / Reguliatsiia diametra bedrennoi arterii pri izmeneniiakh skorosti techeniia perfuzionnykh rastvorov.

It was shown in acute experiments on cats that the femoral artery under constant pressure in its lumen changes its diameter in response to variations in the velocity of both the blood and perfusion solutions. This permits the conclusion that chemical factors of the blood are not responsible for dilatation reactions of the large arteries which appear in response to the increases in the flow rate.

[Optimal structure of the arterial network of skeletal muscles]. / Optimal'naia struktura arterial'noi seti skeletnykh myshts.

A criterion of the optimal structure of muscle arterial network consisting in the minimization of its hydraulic resistance is proposed. Application of this criterion allows one to determine the relationship between the mean values of diameters of vessels of different "orders of branching". Dependence of hydraulic resistance, volumes, blood-flow velocity and pressure in vessels of various calibres on the number of the "order of branching" was established. Rough quantitative estimates are given for the potential increase in the bloodflow of the working muscle as compared to the resting one.