[Changes in blood flow in vessels of the inferior vena cava region under negative intrathoracic pressure].
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Biomedical subjects
Publications and source records attributed to B I Tkachenko.
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In the rostral part of medullary ventral areas (MVA) both the pace-maker neurons forming the tonic sympathetic activity, and the relay structures integrating the baroreceptor information on its way towards vascular areas, are located. The structures of the caudal portion of this cerebral area exert a depressing effect upon the activity of neuronal pools of the brain rostral part and modulate own baroreflexes. An obvious relationship was revealed between the character the extension of changes in the resistive function of the intestine and skeletal muscles' vessels, on the one hand, and the functional state of the MVA structures (excitation or inhibition), on the other hand.
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Pulmonary arteries and veins reacted by constriction to electric activation of rostrally located medulla oblongata ventral structures (lateral paragiant-cell nucleus area) in acute cat experiments. In contrast to this, electric stimulation of medulla oblongata caudal ventral structures induced dilatation of lesser circulation vessels. Counter-phase changes in parameters characterizing pulmonary microhemodynamics (capillary hydrostatic pressure, capillary filtration index) in response to electric stimulation of the studied brain structures permit a conclusion on the high homeostatic parameters of pulmonary microcirculation when maintaining ventilation perfusion relationships.
Under conditions of perfusion of the small intestine's vessels with constant volume of the auto-blood, stationary shifts of the arterial perfusion pressure by +/- 50 mm Hg and/or blood flow by +/- 50% of the initial level practically did not affect the size of the exchange surface of the organ's microvessel bed (the capillary filtration coefficient) or the average capillary pressure in artificially stabilised pressure of venous outflow at the level of 6 mm Hg. However, under conditions of normo-, hypo- and hypertone of the small vessels' smooth muscles, the shifts of the venous outflow pressure (from 0 to 24 mm Hg) increased the exchange surface of the microvessels and the average capillary pressure. The mechanisms of the shifts in microhemodynamics and transcapillary exchange of fluid are discussed.
The experiments on urethane-anesthetized cats with the electrically stimulated ventral brain stem revealed that caudal ventral medulla at the depth of 1500 microns possesses structures whose electrical activation increases the level of carbon dioxide in arterial blood and in the end portion of expirate, on the one hand, and decreases the oxygen content in expirate and arterial blood, on the other hand.
In cats, when perfusing hemodynamically isolated liver with a constant blood volume, an increasing of arterial as well as portal blood flows was shown to increase hydrostatic pressure in sinusoids and lymph production in the liver, whereas decreasing of the flows decreased these parameters. The above changes of the blood flows entailed various shifts of sinusoidal hydrostatic pressure and postsinusoidal resistance. When the volume blood flow in the liver artery increased, the coefficient of sinusoidal filtration increased too, whereas an increment of the blood flow in portal vein led to its diminishing. The resistance of liver artery and portal vein changed very little both in case of increasing and diminishing of the blood flow in these vessels.
The direction and obviousness of changes in systemic arterial and venous vascular beds occurring in combined action of two similarly acting pressor and depressor vasoactive drugs, were studied in acute experiments in cats. The changes of last and general peripheral resistance of vessels were greater under the action of the two drugs as compared to the effect of a single drug, and yet less obvious than their algebraic sum. The shifts in cardiac output and venous return were not greater than the most obvious response to a single drug. The same was true for the blood flow changes in v. v. cavae. Irrespective of the mechanism of action of vasoactive drugs and the direction of shifts of systemic AP, single and combined drugs increased the blood flow in the v. cava anterior whereas the v. cava posterior's blood flow changed in different directions.
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Modelled venous insufficiency of the hind limbs of cats (ligation of the posterior vena cava for 4-6 weeks) led to structural reorganization of the venous walls of the gastrocnemius muscle, which was manifested by a sharp increase of stretchability of the venous bed of the muscle if the activity of the smooth muscles was removed by papaverine, and by significant loss of the sensitivity of the smooth muscles of the intramuscular veins to noradrenaline as regards function. The range of adrenergic changes of postcapillary resistance and capillary pressure was reduced sharply in animals with venous insufficiency. This may be among the causes of disorders of metabolic processes in the skeletal muscles in venous insufficiency.
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A procedure involving the parallel perfusion of deep veins in a cat shank preparation with endogenous blood and a constant volume of dextran solution has been devised. The dextran is supplied to these deep veins via superficial and communicator veins (venae communicantes). With this method it is possible to record dynamic changes in the resistance of the deep veins (postcapillary resistance) in response to intraarterial administration of vasoactive agents into the vascular bed of the shank. Data are presented which indicate that the number of deep veins involved in the changes in venous resistance is equivalent to 67% of the total capacity of the vascular bed of the shank. It is shown that the increase in venous perfusion pressure caused by infusion of noradrenaline into the vascular bed of the shank is essentially equivalent to the increase in mean capillary pressure as determined isovolumetrically. With this new method it is demonstrated for the first time that angiotensin II causes constriction of the deep veins of the shank and that isoproterenol causes dose-dependent dilatatory reactions in the veins within the muscle preparation.
In regimen of the constant blood flow perfusion of shank and small intestine of cat combined effect of hypoxia (10% O2 in N2) and hypothermia (about 30 degrees C) involved a decrease in precapillary resistance, an increase in capillary filtration coefficient in both vascular regions, an increase in postcapillary resistance and in mean capillary pressure in the intestine, and their decrease in the shank. In hypothermia, the hypoxic stimulus induced insignificant shifts in all the parameters under study in both organs. Dependence of hypoxic changes of macro- and microhemodynamics on the activity of adrenergic receptors in the cooled organism was studied on decentralized shank of cat. After cooling of cat and blockade of alpha-adrenoreceptors hypoxic hypoxia caused much greater reduction of precapillary resistance of shank, more striking (by 3 times) increase of capillary filtration coefficient and the increase of capillary pressure and postcapillary resistance in contrast with their decrease to hypoxia under hypothermia before alpha-blockade. Beta-adrenoreceptor blockade had no influence on the changes of the resistance and exchange function of skeletal muscle (shank) blood vessels evoked by hypoxia under cooling. Systemic arterial pressure are diminished during hypoxia under the normothermic conditions of animals. Such kind shifts caused especially by the decreasing of the total peripheral resistance; cardiac output are small raised in this situation. But combined influence of hypoxia and hypothermia evoked the pressor shifts of the systemic arterial pressure because of less decrease of total peripheral resistance and more remarkable rise of cardiac output. Hypoxic stimulus caused both in normothermia and hypothermia conditions caused the rising of venous return.(ABSTRACT TRUNCATED AT 250 WORDS)