Hemodynamic mechanisms of blood flow regulation in the vena cava anterior

A similarity of the blood flow shifts in response to every single pressor or depressor stimulus in the v. cava anterior in cats and a possibility of dissimilar changes of capacity of the vein's vascular basin under the effect of one and the same stimulus, are revealed. This dissimilarity is mainly due to a skin-muscular component of this vascular basin. An increase in the central venous pressure from 0 to 40 mm of water limits the extent of shifts in the capacity function of the v. cava anterior's basin. The blood flow changes in the v. cava anterior is mainly due to a relationship among regional components of the vessels' total peripheral resistance. A potential possible contribution of the v. cava anterior basin vessels capacitance's shifts constitutes 17.5%, whereas under the effect of neurogenic stimuli in the increase of the blood flow in the v. cava anterior may be completely (up to 100%) maintained by a drop of the capacitance of the vein's vascular basin.     

Haemodynamic structure of the venous return changes in action of pressor neurogenic and humoral stimuli upon the circulation system

In cats, constancy of blood flow changes was found in the anterior vena cava under the effect of pressor neurogenic and humoral stimuli. The latter proved to be more efficient in their effect. In the pressor systemic responses, changes of the blood flow in the anterior vena cava yielded the greates contribution.     

Participation of the cava vein blood flow in forming the total venous return under influence of different modality stimuli on the circulation system

Participation of the anterior and posterior veins cava in forming the total venous return under pressor and depressor effects, stimulation of depressing foci of the medulla's ventral part, enhancement of pulmonary ventilation, hypoxia, hypothermia, administration of acetylcholine, histamine, corinfar, was shown to depend on the blood flow shift direction in each of the veins cava, dynamics of shifts' development in time, and intensity of the stimulus. In systemic responses, the blood flow shifts in the vena cava anterior much contribute to the total venous return at the maximum of the systemic arterial pressure rise (r = 0.87) whereas contribution of the vena cava posterior is the greatest during a later occurring increase in the venous return (r = 0.84). Along with increase in the stimulus intensity the vena cava anterior's part in forming the venous return becomes more limited whereas that of the vena cava posterior is enhanced.     

Correlations between changes of the right and left atrial pressures following intravenous injections of pressor and depressor drugs in cats

In acute experiments on anesthetized cats, intravenous injection of the pressor drugs (epinephrine and norepinephrine) and depressor drugs (acetylcholine, histamine, isadrin) caused different changes of right and left atrial pressures. Following catecholamine injection, right atrial pressure decreased in most cases, whereas left atrial pressure increased. In case of injection of the depressor drugs, right atrial pressure increased in most cases, and left atrial pressure decreased. Thus, changes of atrial pressures following intravenous injections of pressor and depressor drugs were reciprocal. The percent changes of the right atrial pressure in case of intravenous injections of pressor drugs were lesser than in the left atrial pressure. In case of intravenous injection of depressor drugs, if both right and left atrial pressures were decreased, then the percent changes of the right atrial pressure were more significant than in the left atrial pressure. If both right and left atrial pressure were increased their percent changes were equal. The increasing of inferior vena cava flow following catecholamine injection was less significant if atrial pressures were increased, whereas in case of depressor drugs injection superior vena cava flow was less significant if atrial pressures were increased. The character of changes of the right and left atrial pressures had no linear correlation with the directions of the shifts of the venous return and cardiac output.     

Character of arterial pressure changes under combined action of pressor and depressor agents

It is shown in acute experiments in cats that byphasic arterial pressure changes occurred due to action of two heterodirectional and equivalent humoral stimuli. Magnitudes of both initial depressor and following pressor phases were authentically less than the ones due to separate action of those stimuli. It is noticed that the character of sum reaction depends neither on action mechanisms of vasoactive agents in the blood circulation system nor differences in the latent period of the effect of those drugs, but connected with intensiveness of stimuli. Predominance of depressor phase magnitude was shown to observe due to a rise of stimuli intensiveness down to complete disappearance of pressor reaction.     

Endothelium-dependent mechanism of formation of the systemic hemodynamics responses

In anaesthetised rats, effects of blockade of the NO-synthetase upon hemodynamic shifts were studied (arterial pressure, cardiac output, general peripheral vascular resistance), the shifts being evoked either by increase (infusion of polyglucon) or by decrease (orthostasis) in the cardiac output. Under the blockade of the NO-synthetase, the pressor effects of polyglucon increased by 27% and the orthostatic hypotension by 72%. Responses of general peripheral vascular resistance changed in the same direction. The findings suggest importance of the NO secretion by the vessels' endothelium for formation of the systemic hemodynamics responses.     

The role of vagus nerves in different changes of the right atrial pressure following intravenous injection of pressor vasoactive drugs

In acute experiments on anesthetized cats, intravenous injection of the norepinephrine and angiotensin caused different changes of right atrial pressure in intact animals (decreasing--I group, of animals, and increasing--II group). After right and left vagus nerves had been cut, the right atrial pressure in the I group of animals decreased, but its changes were lesser than in intact animals due to slowing down of the increase of the right ventricular myocardial contractility and venous return. The latter was the result of severe diminution of the increase of the superior vena cava flow compared with the intact animals, meanwhile the value of the inferior vena cava flow did not change. In the II group animals after vagotomy and intravenous injection of the noripinephrine and angiotensin the sign of the right atrial pressure became negative, i. e. the direction of its shifts changed to the opposite, compared with intact animals. In this case, the changes of the sign of the right atrial pressure was caused by the removal of the reflectory inhibitory vagal influences on the heart, because the values of the right ventricular myocardial contractility and venous return were the same as in intact animals of the group, due to decreasing of the value of the superior vena cava flow and increasing of the shifts of the inferior vena cava flow. The vagotomy alone caused also different changes (decreasing or increasing) of right atrial pressure following increasing of the right ventricular myocardial contractility, meanwhile the changes of the venous return were insignificant. Direct electrical stimulation of both the right and the left vagus nerves caused the increasing of the right atrial pressure and decreasing of the right ventricular myocardial contractility and venous return. Thus we concluded, that different changes of the right atrial pressure in animals following intravenous injection of the pressor vasoactive drugs could be the result of different manifestations of the vagal afferent impulsation, which has influence on the sympathetic tonic discharges on the vessels of the regions of the superior and inferior vena cava, and the vagal reflectory inhibitory influences on the heart.     

Hemodynamics mechanisms of changes in the right atrial pressure following intravenous injection of the depressor drugs

Changes of the right atrial pressure, superior and inferior vena cava flows, right ventricular myocardial contractility (first derivate of right ventricular pressure, dP/dt max) following i.v. injection of acetylcholine, histamine and isoproterenol, were studied in acute experiments on anaesthetized mongrel cats with artificial lung ventilation and opened chest. The right atrial pressure in those cases could be increased (I group of animals) or decreased (II group). In maximal shifts of right atrial pressure following acetylcholine injection, the superior vena cava flow increased but the inferior vena cava flow decreased in equal proportion. When the right ventricular myocardial contractility decreased more than the right atrial pressure was augmented, and when the cardiac negative inotropic effect was weak, the right atrial pressure was reduced. After histamine injection in both groups of animals, right ventricular myocardial contractility was increased on the same level, and changes of the inferior vena cava flow were insignificant. The right atrial pressure was elevated following greater increase of superior vena cava flow. Isoproterenol caused the positive cardiac inotropic effect and augmenting of the superior vena cava flow in both groups of animals. The right atrial pressure was elevated if the inferior vena cava flow increased and, on the other hand, when the inferior vena cava flow decreased the right atrial pressure was reduced. Thus different maximal changes of the right atrial pressure following i.v. injection of acetylcholine, histamine and isoproterenol could be explained by different hemodynamic mechanisms of the interaction between superior and inferior vena cava flow shifts and changes of the right ventricular myocardial contractility.     

Status of the circulatory bed of the vascular membrane of the eyeball and retrobulbar structures during experimental venous stasis

In 43 test animals the state of the blood bed in the retrobulbar formations and the eyeball vasular tunic has been studied under venous congestion produced by ligation of the anterior vena cava (in dogs) and both external jugular veins (in rabbits). A complex of histological, histotopographic, morphometric and variation-statistical techniques has been used. The results obtained demonstrate that disturbances in the venous outflow in the anterior vena cava system produce certain responses in all parts of the retrotubular adipose tissue, of the eyeball muscles, of the optic nerve tunics, of the vascular tunic. Certain stageness is noted in the course of venous congestion. Places of the greatest morphological changes in the eyeball vascular tunic are determined. They are zones of vorticose veins formation and the area corresponding to the posterior pole of the eyeball. The analysis of the specific areas of the intermuscular arteries and veins cross sections demonstrates that in the reaction of these vessels to the different venous outflow in the anterior vena cava system these is certain unevenness in different ofthalmic muscles.     

Systemic and renal hemodynamic responses to vascular blockade of vasopressin in conscious dogs with ascites

A role for arginine vasopressin has been implicated in the compensatory control of arterial blood pressure in several animal models with reported increases in plasma levels of arginine vasopressin. A threefold elevation in plasma vasopressin has been reported in conscious dogs following constriction of the inferior vena cava. In the present study, infusion of the arginine vasopressin antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine] Arg8-vasopressin into conscious dogs with chronic caval constriction did not decrease mean arterial blood pressure. However, the dose of infused antagonist completely blocked the pressor response to 2 micrograms of exogenous vasopressin. Also the antagonist produced no effect on heart rate, plasma renin activity, or urinary volume and electrolyte excretions. A slight, transient increase (P less than or equal to 0.05) was observed in creatinine clearance and in PAH clearance following antagonist infusion, suggesting a possible decrease in renal vascular resistance. These data suggest that the direct vasoconstrictor actions of vasopressin contribute minimally, if at all, to blood pressure maintenance following chronic caval constriction. Alternatively, blockade of endogenous vasopressin receptors at the level of peripheral arterioles may have resulted in no depressor response due to a masking of this response by other compensatory hormonal and neural pressor systems.     

Changes in pressor and depressor reactions following partial pancreatectomy]

Experiments were conducted on 39 mongrel pubertal dogs. The course of pressor and depressor reactions under conditions of normal vital activity and after partial corporocaudal resection of the pancreas was studied. The principal indices characterizing the changes of pressor reaction to noradrenaline, and of the depressor one -- to bradykinin and kallikrein before and 10 to 12 days after the corporocaudal resection of the pancreas were determined. Resection of the corporo-caudal part of the pancreas intensified the pressor reactions to noradrenaline, and depressor ones to bradykinin and kallikrein; it increased the initial negative chronotropic effect of catecholamines on the heart, and also enhanced the positive chronotropic effect of noradrenaline, kallikrein and bradykinin on the heart.     

Influence of tone on responses to acetylcholine in the rabbit pulmonary vascular bed

Pulmonary vascular responses to acetylcholine were compared under resting and high tone conditions of the intact-chest rabbit. Under resting tone conditions, intralobar injections of acetylcholine increased lobar arterial pressure in a dose-related manner. The pressor responses to acetylcholine under resting conditions were blocked by meclofenamate, indomethacin, atropine, and pirenzepine. When lobar vascular resistance was raised to a high steady level, low doses of acetylcholine decreased lobar arterial pressure, whereas higher doses elicited a biphasic response with the pressor component predominating at the highest dose studied. Under high tone conditions, only the pressor component of the response was blocked by meclofenamate or indomethacin, whereas pressor and depressor responses were blocked by atropine or the 600-micrograms/kg iv dose of pirenzepine. Pressor responses to acetylcholine under resting and high tone conditions were blocked by pirenzepine (50 micrograms/kg iv), whereas gallamine had no effect on responses to acetylcholine. The 50-micrograms/kg iv dose of pirenzepine had no effect on depressor responses or the depressor component of the response to acetylcholine. The present data support the concept that acetylcholine has significant cyclooxygenase-dependent pressor activity in the rabbit pulmonary vascular bed and suggest that this response is mediated by a muscarinic M1-type receptor. These data also show that, under high tone conditions, a vasodilator response or a vasodilator component of a biphasic response is unmasked. This response is not dependent on the release of cyclooxygenase products and is mediated by a muscarinic receptor that is neither of the M1- nor the M2-type.     

The constant level of the right atrial pressure and its role in the venous return characteristics]

Dynamics of the central venous pressure, superior and inferior v. cava flow and venous return following action of pressor stimuli were studied in acute experiments on anaesthetised mongrel cats with artificial lung ventilation and opened chest. The central venous pressure returned to the initial level faster as compared with the dynamics of superior and inferior v. cava flow and venous return. The superior v. cava blood flow increased more than that of inferior v. cava. The data suggest that the central venous pressure is controlled near the lower constant level.     

The role of the cardiac-pulmonary blood volume in the changes in left ventricle output during stimulation of the afferent fibers of somatic nerves

Stimulation of tibial nerve afferent fibers has revealed heterogeneous shifts of left ventricular output, as well as pulmonary artery and posterior vena cava blood flow in anesthetized cats. Uniform changes in left ventricular output and pulmonary artery blood flow were noted in the majority of cases, with venous return most often exceeding pulmonary artery blood flow. beta-adrenoreceptor blockade failed to influence changes in pulmonary artery blood flow. It is concluded that the increase in pulmonary artery blood flow depends on the rise in venous return, but not on neurogenic influence upon the right ventricle. The reduction in left ventricular output is the result of decreased right ventricular outflow due to its overload caused by pulmonary vasoconstriction.     

Genetically determined variation in the azygos vein in the mouse.

The normal mouse is expected to have a single and left-sided azygos vein that develops from the paired embryonic cardinal venous system and drains most of the right and left thoracic walls into the left anterior vena cava. During routine autopsies of adult mice, most individuals of the C57BL/6J strain were found to have this pattern but a distribution of different azygos venous patterns was found in the WB/ReJ strain. In WB/ReJ the patterns varied from a single unpaired vein on the right side that connected to the right anterior vena cava through bilaterally symmetrical and paired veins to the expected unpaired vein on the left side. A classification scheme for the observed patterns of azygos veins was developed and the frequency distributions of C57BL/6J and WB/ReJ mice in these classes were compared. The strain difference in the azygos venous system between C57BL/6J and WB/ReJ can be interpreted as a genetically determined threshold trait of development. Beginning with a paired and symmetrical cardinal venous system, the C57BL/6J genotype shifts to a left-sided azygos pattern but the WB/ReJ genotype remains with a more bilateral azygos pattern. Genetic study of this azygos trait will be useful for the study of lateral asymmetries in mammalian development and for the interpretation of venous heterotaxies (anomalous placement of veins) in the mouse that are found in association with mutations such as situs inversus viscerum (iv) and dominant hemimelia (Dh).     

Ostium of the collection stem of the anterior cardiac veins (vv. cardiacae anteriores) in the vena cava, inferior

In 1 of 150 studied cases, we found the collection stem of anterior cardiac veins that emptied into the inferior vena cava. This collection stem had eight tributaries: two right atrial veins, five anterior cardiac veins and a right marginal vein. The caliber of the collection stem was increasing gradually from its beginning (2.8 mm) to its orifice (4.5 mm). The orifice of the collection stem was in the inferior vena cava, at a distance of 10 mm from its ostial valve, and was itself provided with a semilunar valve.     

Interaction between depressor and pressor reflexes arising from the aorta in dogs

In 18 dogs anesthetized with morphine-chloralose the interaction between the aortic nerve (AN) pressor and depressor reflexes was studied. Low-intensity, high-frequency electrical stimulation of the AN causes large decreases in heart rate and systemic pressure characteristic of baroreflex responses. High-intensity, low-frequency stimulation of the AN causes modest increases in heart rate and systemic pressure similar to the responses observed to intraaortic nicotine. Simultaneous electrical stimulation of these antagonistic reflexes results in much smaller (P less than 0.001) reductions in heart rate and systemic pressure that can be explained on the basis of simple addition of the individual responses. Similarly the AN depressor reflexes are suppressed during intraaortic infusions of nicotine (40 micrograms/min). The results suggest that the inhibitory effects of the AN baroreflexes are suppressed by the aortic chemoreflexes . This interaction occurs in the CNS rather than at the level of the heart or vascular smooth muscle.     

边缘前脑内重要升、降压区调节血压的机制

边缘前脑在调节情绪和应激反应、水和电解质平衡中起重要作用。这些活动都伴有心血管活动的变化。边缘前脑内很多升、降压区参与这些活动。近年来随着脑干各区调节血压机制研究的深入,边缘前脑调节血压机制的研究也有很大进展。本文综述了边缘前脑各升、降压区间,以及它们及脑干各区间的机能联系及参与的递质和受体。     

Contribution of AMPA/kainate receptors in the rostral ventrolateral medulla to the hypotensive and sympathoinhibitory effects of clonidine

The depressor and sympathoinhibitory effect of the imidazoline drug clonidine is reported to be associated with functional states of the central glutamate receptors. The rostral ventrolateral medulla (RVLM) has been recognized as a specific target area for mediating the central depressor mechanism of clonidine. The objective of this study was to determine the role of the glutamate receptor subtype alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor within the RVLM in clonidine-induced depressor and sympathoinhibitory action in anesthetized normotensive rats. Unilateral microinjection of 200 pmol of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a potent AMPA/kainate receptor antagonist, into the RVLM completely abolished the pressor action evoked by AMPA (5 pmol) without affecting the pressor action of N-methyl-D-aspartate (20 pmol). Pretreatment with intra-RVLM injection of CNQX (20 and 200 pmol) dose dependently attenuated the reduction in blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) elicited by intra-RVLM clonidine (5 nmol) or intravenous clonidine (10 microg/kg), while 2 pmol of CNQX did not alter clonidine-induced cardiovascular action. Furthermore, the decreases in BP, HR, and RSNA evoked by intravenous clonidine (10 microg/kg) or intra-RVLM clonidine (5 nmol) were reversed when CNQX (20 and 200 pmol) was subsequently injected into the RVLM. In conclusion, these data show that blockade of AMPA/kainate receptors in the RVLM significantly antagonizes decreases in BP, HR, and sympathetic activity induced by clonidine, suggesting that the AMPA/kainate receptors within the RVLM contribute to the depressor and sympathoinhibitory effect of clonidine.     

Stimulation of NTS A1 adenosine receptors evokes counteracting effects on hindlimb vasculature

Our previous studies concluded that stimulation of the nucleus of the solitary tract (NTS) A2a receptors evokes preferential hindlimb vasodilation mainly via inducing increases in preganglionic sympathetic nerve activity (pre-ASNA) directed to the adrenal medulla. This increase in pre-ASNA causes the release of epinephrine and subsequent activation of beta-adrenergic receptors that are preferentially located in the skeletal muscle vasculature. Selective activation of NTS A1 adenosine receptors evokes variable, mostly pressor effects and increases pre-ASNA, as well as lumbar sympathetic activity, which is directed to the hindlimb. These counteracting factors may have opposite effects on the hindlimb vasculature resulting in mixed vascular responses. Therefore, in chloralose-urethane-anesthetized rats, we evaluated the contribution of vasodilator versus vasoconstrictor effects of stimulation of NTS A1 receptors on the hindlimb vasculature. We compared the changes in iliac vascular conductance evoked by microinejctions into the NTS of the selective A1 receptor agonist N6-cyclopentyladenosine (330 pmol in 50 nl volume) in intact animals with the responses evoked after beta-adrenergic blockade, bilateral adrenalectomy, bilateral lumbar sympathectomy, and combined adrenalectomy + lumbar sympathectomy. In intact animals, stimulation of NTS A1 receptors evoked variable effects: increases and decreases in mean arterial pressure and iliac conductance with prevailing pressor and vasoconstrictor effects. Peripheral beta-adrenergic receptor blockade and bilateral adrenalectomy eliminated the depressor component of the responses, markedly potentiated iliac vasoconstriction, and tended to increase the pressor responses. Lumbar sympathectomy tended to decrease the pressor and vasoconstrictor responses. After bilateral adrenalectomy plus lumbar sympathectomy, a marked vasoconstriction in iliac vascular bed still persisted, suggesting that the vasoconstrictor component of the response to stimulation of NTS A1 receptors is mediated mostly via circulating factors (e.g., vasopressin, angiotensin II, or circulating catecholamines released from other sympathetic terminals). These data strongly suggest that stimulation of NTS A1 receptors exerts counteracting effects on the iliac vascular bed: activation of the adrenal medulla and beta-adrenergic vasodilation versus vasoconstriction mediated by neural and humoral factors.