Hemodynamic mechanisms of the pulmonary artery pressure and blood flow changes following vasoactive pressor drugs injection

The character and values of changes of the pulmonary and systemic hemodynamics following epinephrine, norepinephrine and angiotensin intravenous injection were studied in acute experiments on the anesthetized cats. After catecholamines injection pulmonary blood flow was always increased, meanwhile pulmonary artery pressure can be elevated (in the most observations) or decreased. In the cases of angiotensin administration the pulmonary blood flow could be augmented or decreased; pulmonary artery pressure had been increased or decreased independently from the character of changes of pulmonary flow. Thus, linear correlation between shifts of the pulmonary artery pressure and pulmonary blood flow had not been revealed. The changes of the pulmonary artery pressure were not correlated with the pulmonary vascular resistance ones; however they had strong relationship with the changes of the left atrial pressure. If the left atrial pressure was decreased the pulmonary artery pressure elevation was less, comparing with its values in experiments, where the left atrial pressure was increased; in the case of depressor shifts of pulmonary artery pressure, the left atrial pressure was also decreased. The character and values of the pulmonary blood flow changes were strongly correlated with the changes of the venous return; however they had no linear correlations with the right and left atrial pressures and pulmonary vascular resistance changes. Thus we concluded, that hemodynanics mechanisms of the pulmonary artery pressure and flow changes following vasoactive pressor drugs injection changes are different.     

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.     

The pulmonary hemodynamics changes under experimental myocardial ischemia in rabbits following increased arterial pressure

In acute experiments in anesthetized rabbits, changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied in control animals and after the infusion of adrenaline and phenylephrine. The pulmonary artery pressure was increased following infusion of these drugs; however, it decreased to normal level in the condition of myocardial ischemia. Meanwhile the pulmonary vascular resistance was elevated to the same level in both cases. Following adrenaline infusion, the pulmonary artery blood flow and venous return increased and, in the condition of myocardial ischemia, they decreased to normal level, but the left atrial pressure was decreased. Following phenylephrine infusion, the pulmonary artery blood flow and venous return did not change and, in the condition of myocardial ischemia, these parameters decreased lower than normal level but the left atrial pressure was elevated. Thus we concluded that equal values of the pulmonary artery pressure in both cases were caused by changes of different character in the left atrial pressure. The differences of the changes character and values of the pulmonary artery flow under experimental myocardial ischemia following the infusion of adrenaline and phenylephrine were caused by different shifts of the venous return.     

Correlations between changes of the right and left atrial pressures and systemic hemodynamics parameters following catecholamines intravenous injections in cats

In acute experiments on anesthetized cats, intravenous injection of epinephrine and norepinephrine caused different changes of right and left artrial pressures. These shifts mostly (82%) had similar directions: in these experiments, both right and left atrial pressures could be decreased (I group of animals) or increased (II group). The number of animals in these groups was equal. However, in 18% of the experiments, right atrial pressure was decreased, while left atrial pressure was increased. The changes of the left atrial pressure was, as a rule, more significant as compared with right atrial pressure shifts. In the I group of animals, systolic right atrial pressure was not changed, and systolic left atrial pressure was decreased. In the II group of animals, systolic pressure in both atria was augmented. Diastolic pressure was decreased in both atria in all the animals. When the atrial pressures were decreased, the increases of the superior and inferior vena cava flows, venous return and cardiac output were more significant as compared with animals in which the atrial pressures had been elevated. The changes of the superior and inferior vena cava flows were more obvious in animals following epinephrine injection as compared with animals in which norepinephrine was injected. The right atrial pressure returned to the initial level more rapidly than the left atrial pressure, and the time dynamics of the shifts of the right atrial pressure was similar to that of the superior vena cava flow. The temporal changes of the left atrial pressure were identical to the time changes of the cardiac output. We concluded that character of changes of the mean, systolic, and diastolic right and left atrial pressures following catecholamines injections was not correlated with the direction of venous return and cardiac output shifts, and was depending on intracardiac hemodynamics.     

Relations between changes of the pulmonary and systemic hemodynamics following neurogenic stimuli

The character and values of changes of the pulmonary and systemic hemodynamics following neurogenic stimuli application on the cardiovascular system were studied in acute experiments on the anesthetized cats. Vagus nerve stimulation reduced the heart rate and decreased myocardial contractility in result, right and left atrial pressure increased, whereas pulmonary pressure and flow, venous return, cardiac output and venous return decreased. Pulmonary pressure reached maximal level and returned to the initial value earlier than the pulmonary flow. On the contrary, pulmonary pressure, following neurogenic pressor stimuli, reached maximal level and returned to the initial value later than the pulmonary flow; the sign of the changes of the pulmonary pressure could be positive or negative, whereas pulmonary flow were always increased. The venous return did not change, and for this reason it could not cause the increasing of pulmonary flow which was elevated following increasing of the heart rate and myocardial contractility. The shifts of the pulmonary pressure were correlated with the pulmonary resistance those, which were increased after the stellate ganglion stimulation and decreased following carotid reflex; they did not change in case of sciatic nerve stimulation. The shifts of the pulmonary pressure did not depended on the decreased right and left atrial pressures. When the pulmonary flow was always increased, the cardiac output following electrical stimulation of the stellate ganglion and sciatic nerve was elevated, and it was decreased following carotid reflex, i. e. linear correlation between these parameters were not found. Pulmonary and systemic arterial pressure changes were more obvious in case of direct neurogenic stimuli application comparing with reflectory ones; in both cases, the positive chrono- and inotropic cardiac effects were similar.     

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.     

Influence of lung volume and left atrial pressure on reverse pulmonary venous blood flow

Infarction of the lung is uncommon even when both the pulmonary and the bronchial blood supplies are interrupted. We studied the possibility that a tidal reverse pulmonary venous flow is driven by the alternating distension and compression of alveolar and extra-alveolar vessels with the lung volume changes of breathing and also that a pulsatile reverse flow is caused by left atrial pressure transients. We infused SF6, a relatively insoluble inert gas, into the left atrium of anesthetized goats in which we had interrupted the left pulmonary artery and the bronchial circulation. SF6 was measured in the left lung exhalate as a reflection of the reverse pulmonary venous flow. No SF6 was exhaled when the pulmonary veins were occluded. SF6 was exhaled in increasing amounts as left atrial pressure, tidal volume, and ventilatory rates rose during mechanical ventilation. SF6 was not excreted when we increased left atrial pressure transients by causing mitral insufficiency in the absence of lung volume changes (continuous flow ventilation). Markers injected into the left atrial blood reached the alveolar capillaries. We conclude that reverse pulmonary venous flow is driven by tidal ventilation but not by left atrial pressure transients. It reaches the alveoli and could nourish the alveolar tissues when there is no inflow of arterial blood.     

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.     

Wedge pressure in large vs. small pulmonary arteries to detect pulmonary venoconstriction

Pulmonary arterial wedge pressure measures the pressure where blood flow resumes on the venous side. By occlusion of a large artery, the point where blood flow resumes will be in or near the left atrium. However, by occlusion of a small artery, it is possible to shift the point where flow resumes to a more proximal site in the veins and thus measure a pressure within the small veins. Increased pulmonary venous pressure, as a result of partial obstruction in the large veins, may not be detected by wedging a Swan-Ganz catheter in a large artery but may be detected by wedging in a small artery. We demonstrated this phenomenon in open-chest dogs by mechanically obstructing the left lower lobar vein or by infusing histamine to cause a generalized pulmonary venoconstriction. The wedge pressure measured by a 7-F Swan-Ganz catheter, with its balloon inflated in the main left lower lobar artery, nearly equaled left atrial pressure. On the other hand, the wedge pressure measured with a 7-F, 5-F, or a PE-50 catheter advanced into a small artery (without a balloon) was considerably higher than left atrial pressure. These results suggest that high resistance in the pulmonary veins can be demonstrated with the Swan-Ganz catheter by comparing the pressures obtained with the catheter wedged in a small and large artery.     

Experimental ductus arteriosus: the relationships of atrial pressure, dilatation and flow with ANF secretion

The design of the study was to determine whether an increased blood flow as seen in shunt lesions could serve as a stimulus for the secretion of atrial natriuretic factor (ANF). Since atrial pressure, flow, and dilatation are closely related, an experimental ductus arteriosus model was utilized, in which acute changes of flow are assumed not to dilate the left atrium. In six dogs, a Dacron graft was constructed between the main pulmonary artery and the innominate artery. Constricting and releasing the tape around the graft adjusted the amount of "ductal" shunting. The total pulmonary flow and the shunt flow were measured by electromagnetic-flow transducers around the aortic root and around the graft. Plasma ANF concentration was measured from both cardiac atria. The size of the left atrium was determined from echocardiographic measurements made from a short-axis view. The total pulmonary flow varied between 1.2 and 5.8 1/min. The highest measured ANF was 396 pg/ml, and this was from the left atrium when the pressure was 18 mmHg, the highest left atrial pressure recorded. The highest right atrial pressure (5 mmHg) also correlated with the highest right-atrial level of ANF (366 pg/ml). The right atrial pressure had a significant correlation with plasma ANF concentration (R = 0.43, p less than 0.05). Pulmonary flow and plasma ANF concentration did not correlate; neither did left atrial size and ANF levels in 16 flow states where the size was measured. In the absence of atrial dilatation there was minimal stimulus for ANF secretion. A transient increase of left atrial pressure, without a concomitant significant atrial dilatation, did not serve as a significant stimulus for ANF secretion.     

Furosemide reduces lung fluid filtration in lambs with lung microvascular injury from air emboli

To study the effects of furosemide on the neonatal pulmonary circulation in the presence of lung injury, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine lambs that received furosemide, 2 mg/kg iv, during a continuous 8-h intravenous infusion of air. Air embolism increased pulmonary vascular resistance by 71% and nearly tripled steady-state lung lymph flow, with no change in lymph-to-plasma protein ratio. These findings reflect an increase in lung vascular protein permeability. During sustained lung endothelial injury, diuresis from furosemide led to a rapid reduction in cardiac output (average 29%) and a 2-Torr decrease in left atrial pressure. Diuresis also led to hemoconcentration, with a 15% increase in both plasma and lymph protein concentrations. These changes were associated with a 27% reduction in lung lymph flow. In a second set of studies, we prevented the reduction in left atrial pressure after furosemide by inflating a balloon catheter in the left atrium. Nevertheless, lymph flow decreased by 25%, commensurate with the reduction in cardiac output that occurred after furosemide. In a third series of experiments, we minimized the furosemide-related decrease in cardiac output by opening an external fistula between the carotid artery and jugular vein immediately after injection of furosemide. In these studies, the reduction in lung lymph flow (average 17%) paralleled the smaller (17%) decrease in cardiac output. These results suggest that changes in lung vascular filtration pressure probably do not account for the reduction in lung lymph flow after furosemide in the presence of lung vascular injury.(ABSTRACT TRUNCATED AT 250 WORDS)     

The pulmonary hemodynamic changes under experimental myocardial ischemia in rabbits following beta-adrenoreceptors blockade

In acute experiments in anesthetized rabbits, changes of the pulmonary hemodynamics following myocardial ischemia in the region of the descendent left coronary artery were studied as well as in control animals and after the blockade of beta-adrenoreceptors. The myocardial ischemia decreased the left ventricular myocardial contractility, cardiac output and arterial pressure, decreased the pulmonary artery pressure and flow. Following myocardial ischemia, the pulmonary artery pressure decreased less than pulmonary artery blood flow as the result of elevating of the left atrial pressure, meanwhile pulmonary vascular resistance was not changed. Following myocardial ischemia in animals after the blockade of the beta-adrenoreceptors, the pulmonary flow decreased the same as in control animals. However, the pulmonary artery pressure was decreased twofold more significantly than in control animals, and its diminishing was in the same degree as the pulmonary artery flow. Following myocardial ischemia after the blockade of the beta-adrenoreceptors, the pulmonary vascular resistance decreased whereas the left atrial pressure did not change significantly because the myocardial contractility decreased less than in control animals.     

Changes in venous return parameters associated with univentricular Fontan circulations

To clarify the physiology of venous return (Q(vr)) in Fontan circulations, venous return conductance (G(vr)) and mean circulatory filling pressure (P(mcf)) were determined in pentobarbital sodium-anesthetized pigs. Relationships between Q(vr) and right (biventricular, n = 8) or left (Fontan, n = 8) filling pressures are described by straight lines with significant correlation coefficients. Estimated P(mcf) values were correlated with observed P(mcf) values in either circulations (P 相似文献   

Effect of progressive exercise on lung fluid balance in sheep

The purpose of this study is to determine the roles of cardiac output and microvascular pressure on changes in lung fluid balance during exercise in awake sheep. We studied seven sheep during progressive treadmill exercise to exhaustion (10% grade), six sheep during prolonged constant-rate exercise for 45-60 min, and five sheep during hypoxia (fraction of inspired O2 = 0.12) and hypoxic exercise. We made continuous measurements of pulmonary arterial, left atrial, and systemic arterial pressures, lung lymph flow, and cardiac output. Exercise more than doubled cardiac output and increased pulmonary arterial pressures from 19.2 +/- 1 to 34.8 +/- 3.5 (SE) cmH2O. Lung lymph flow increased rapidly fivefold during progressive exercise and returned immediately to base-line levels when exercise was stopped. Lymph-to-plasma protein concentration ratios decreased slightly but steadily. Lymph flows correlated closely with changes in cardiac output and with calculated microvascular pressures. The drop in lymph-to-plasma protein ratio during exercise suggests that microvascular pressure rises during exercise, perhaps due to increased pulmonary venous pressure. Lymph flow and protein content were unaffected by hypoxia, and hypoxia did not alter the lymph changes seen during normoxic exercise. Lung lymph flow did not immediately return to base line after prolonged exercise, suggesting hydration of the lung interstitium.     

Influence of pregnancy on mean systemic filling pressure and the cardiac function curve in guinea pigs.

To assess the degree of circulatory fullness and to evaluate the influence of peripheral and cardiac factors in the regulation of cardiac output during pregnancy, the following studies were conducted using pentobarbital-anesthetized, open-chest nonpregnant and late term pregnant guinea pigs. Mean circulatory filling pressure was taken as the equilibrium pressure when the pulmonary artery was constricted. Total vascular compliance was assessed by +/- 5-mL changes in blood volume performed while this constriction was maintained. A separate group of guinea pigs was prepared with a pulmonary artery electromagnetic flow probe and right atrial catheter. Rapid infusion of saline was used to increase right atrial pressure while the cardiac output was determined. Pregnancy was characterized by the following changes relative to nonpregnant controls: 51Cr-labelled RBC blood volume increased from 55 +/- 3 to 67 +/- 3 mL/kg; mean circulatory filling pressure increased from 7.1 +/- 0.2 to 8.0 +/- 0.5 mmHg (1 mmHg = 133.322 Pa); right atrial pressure decreased from 3.4 +/- 0.2 to 2.1 +/- 0.3 mmHg; and cardiac output increased from 71.8 +/- 3.9 to 96.8 +/- 3.3 mL.min-1.kg-1. Total vascular compliance was not changed (2.1 +/- 0.1 mL.kg-1.mmHg-1) and most of the expanded blood volume was accommodated as unstressed volume. The cardiac function curve was shifted upwards in pregnant animals. The resistance to venous return, as determined from the slope of the venous return curves, was not changed. These data suggest that the circulation of the pregnant guinea pig is slightly overfilled.(ABSTRACT TRUNCATED AT 250 WORDS)     

Right atrial pressure affects the interaction between lung mechanics and right ventricular function in spontaneously breathing COPD patients

Introduction

It is generally known that positive pressure ventilation is associated with impaired venous return and decreased right ventricular output, in particular in patients with a low right atrial pressure and relative hypovolaemia. Altered lung mechanics have been suggested to impair right ventricular output in COPD, but this relation has never been firmly established in spontaneously breathing patients at rest or during exercise, nor has it been determined whether these cardiopulmonary interactions are influenced by right atrial pressure.

Methods

Twenty-one patients with COPD underwent simultaneous measurements of intrathoracic, right atrial and pulmonary artery pressures during spontaneous breathing at rest and during exercise. Intrathoracic pressure and right atrial pressure were used to calculate right atrial filling pressure. Dynamic changes in pulmonary artery pulse pressure during expiration were examined to evaluate changes in right ventricular output.

Results

Pulmonary artery pulse pressure decreased up to 40% during expiration reflecting a decrease in stroke volume. The decline in pulse pressure was most prominent in patients with a low right atrial filling pressure. During exercise, a similar decline in pulmonary artery pressure was observed. This could be explained by similar increases in intrathoracic pressure and right atrial pressure during exercise, resulting in an unchanged right atrial filling pressure.

Conclusions

We show that in spontaneously breathing COPD patients the pulmonary artery pulse pressure decreases during expiration and that the magnitude of the decline in pulmonary artery pulse pressure is not just a function of intrathoracic pressure, but also depends on right atrial pressure.     

Effect of thoracic duct drainage on hydrostatic pulmonary edema and pleural effusion in sheep

Positive end-expiratory pressure (PEEP) increases central venous pressure, which in turn impedes return of systemic and pulmonary lymph, thereby favoring formation of pulmonary edema with increased microvascular pressure. In these experiments we examined the effect of thoracic duct drainage on pulmonary edema and hydrothorax associated with PEEP and increased left atrial pressure in unanesthetized sheep. The sheep were connected via a tracheostomy to a ventilator that supplied 20 Torr PEEP. By inflation of a previously inserted intracardiac balloon, left atrial pressure was increased to 35 mmHg for 3 h. Pulmonary arterial, systemic arterial, and central venous pressure as well as thoracic duct lymph flow rate were continuously monitored, and the findings were compared with those in sheep without thoracic duct cannulation (controls). At the end of the experiment we determined the severity of pulmonary edema and the volume of pleural effusion. With PEEP and left atrial balloon insufflation, central venous and pulmonary arterial pressure were increased approximately threefold (P less than 0.05). In sheep with a thoracic duct fistula, pulmonary edema was less (extra-vascular fluid-to-blood-free dry weight ratio 4.8 +/- 1.0 vs. 6.1 +/- 1.0; P less than 0.05), and the volume of pleural effusion was reduced (2.0 +/- 2.9 vs. 11.3 +/- 9.6 ml; P less than 0.05). Our data signify that, in the presence of increased pulmonary microvascular pressure and PEEP, thoracic duct drainage reduces pulmonary edema and hydrothorax.     

Quantitative radionuclide assessment of total pulmonary vascular volume changes

Current techniques do not permit continuous and noninvasive assessments of changes in total pulmonary intravascular volume. Hence, the present study was undertaken to determine whether quantitative radionuclide imaging can be used to determine the direction and estimate the magnitude of total pulmonary vascular volume changes. The pulmonary circulation was separately perfused at a constant rate via the pulmonary artery and drained at a constant pressure via the left atrium in nine dogs. Changes in pulmonary intravascular volume were recorded as reciprocal changes in extracorporeal reservoir volume during phenylephrine or isoproterenol administration, a 20% increase in pulmonary artery flow or a 5 mmHg (1 mmHg = 133.32 Pa) decrease in left atrial pressure. Erythrocytes were labeled with technetium-99m and pulmonary volume changes were determined from tissue attenuation, blood radioactivity, and changes in total pulmonary radioactivity obtained with a gamma-camera. During each of the interventions, count changes correlated with volume changes (r greater than or equal to 0.75). The technique reliably detected volume changes as small as 10 mL. For all 531 individual pairs of radionuclide- and reservoir-determined volume changes, the correlation between reservoir-determined and radionuclide-estimated pulmonary intravascular volume changes was 0.87. The standard error of the radionuclide estimate was 21 mL. Hence, the present study demonstrates that quantitative radionuclide imaging can be used to continuously and noninvasively determine total pulmonary vascular volume changes.     

Haemodynamic effects of intravenous morphine in patients with acute myocardial infarction complicated by severe left ventricular failure.

The haemodynamic effects of intravenous morphine sulphate (0.2 mg/kg body weight) were measured in 10 patients with acute myocardial infarction complicated by severe left ventricular failure. Fifteen minutes after morphine injection there was a significant fall in mean heart rate (from 109 to 101 beats/min) and mean systemic arterial pressure (from 80 to 65 mm HG), and a small fall in mean cardiac index (from 2.4 to 2.21/min/m2). Haemodynamic changes at 45 minutes were similar. Neither stroke index nor indirect left ventricular filling pressure (measured as pulmonary artery end-diastolic pressure) were consistently improved 15 or 45 minutes after injection. The useful action of morphine in relieving distressing cardiac dyspnoea is not adequately explained by systemic venous blood pooling. These results suggest that the effects of morphine on the central nervous system are more important.     

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.