Systemic Vascular Capacity Research Articles

A Novel Non-invasive Predictor Measure of Left Atrial Pressure and Practical Implicates in High Frequency Ventilation: Theory.

A new prototype of ventilator mode, based on high-frequency ventilation (HFV), aims to address the interrelations among diverse respiratory variables, several intercardiovascular parameters rapports, and instantaneously the intrarespiratory and cardiac interactions. This article proposes a logarithmic network of integrated correlation ratio H/V, R correlation, that primarily relates both dependent respiratory (V) and independent hemodynamic variables (H). Given a constant steady state of the heart and vasculature, a difference between calculated ratio (R calc), and optimized ratio (R opt) could be utilized to adjust many aspects of several parameters and outcomes in critically ill patients. The central venous pressure (CVP) waveanalysis aims to approachseveral cardiovascular parameters, endpoints of left atrial (LA) pressure, and the cardiac output (CO) with the help of thermodilution curve analysis. This might result in several innovative formulas of mathematical base. Their relevant clinical implicates demonstrated a wide area of normalized distribution capacity (Cd), systemic vascular capacity (Cs), pulmonary vascular capacitance (Cp), pulmonary vascular resistance (PVR), and mean pulmonary artery pressure (MPAP). The authors claim that prepared software programming helps network integration of all these variables, feeding back and addressing the prototypeof novel mode for the oldnew applicationof HFV. One potential unique criterion is adjusting LA and ultimately CO through a feedback control mechanism. Though this all sounds very plausible, the reader must be reminded that everything in this work is based on the most expected speculations and experience and could be potentially different than that in vivo.More importantly, animalexperimental studies are warranted.

The Underestimated Compression Effect of Neoprene Wetsuit on Divers Hydromineral Homeostasis

This study aimed at demonstrating that the neoprene wetsuit provides not only thermal protection. Compression it exerts on the diver's shell significantly impacts hydromineral homeostasis by restraining the systemic vascular capacity and secondarily increasing urine output on dry land and during scuba diving. 8 healthy divers underwent five 2-h sessions: sitting out of water in trunks (control situation), sitting out of water wearing a wetsuit, and 3 wetsuit scuba-immersed sessions at 1, 6 and 12 msw depth, respectively. Urine volumes and blood samples were collected. Hemoglobin (Hb), hematocrit (Ht) and plasma sodium concentration were measured. Interface pressure between the garment and the skin was measured at 17 sites of the body shell, with a pressure transducer. Mean interface pressures between wetsuit and skin amounted to: 25.8±2.8 mm Hg. Whatever the depth, elastic recoil tension of wetsuit material was unchanged by immersion. Weight loss was respectively 2 and 3 times greater when wetsuit was worn out of water (430 g) and during immersion (710 g) than when divers did not wear any wetsuit out of water (235 g; p<0.05). Urine volume accounted for 85% of weight loss in either session. Weight loss and urine volume were similar whatever immersion depth. The decrease in plasma volume amounted to 8% of urine volume when divers did not wear any wetsuit out of water, and to 30% when wetsuit was worn out of water or during immersion. Diving wetsuit develops a pressure effect that alters diver's hydromineral homeostasis. During immersion, the wetsuit pressure merges into the larger main effect of hydrostatic pressure to reduce water content of body fluids, unrelated to immersion depth.

The following letters are in response to the Point:Counterpoint series “Hypoxic pulmonary vasoconstriction is/is not mediated by increased production of reactive oxygen species” that appears in this issue.

To the Editor : The underlying issue being discussed ([1a][1], [4][2]) seems much broader than simply the role of venoconstriction. It is really about the regulation of the magnitude of cardiac output. Thus while the argument put forth by Hainsworth and Drinkhill is fine as far as it goes, it fails

Propofol-induced increase in vascular capacitance is due to inhibition of sympathetic vasoconstrictive activity.

Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity. In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol. The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups. The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.

Alteration of vascular capacitance and blood flow distribution during halothane anesthesia.

We examined the effect of halothane on systemic vascular capacitance as well as on systemic vascular resistance using cardiopulmonary bypass in dogs. Venous outflows from two different vascular beds, the splanchnic and extrasplanchnic beds, were also measured. Under constant perfusion flow and constant central venous pressure, a change in reservoir blood volume inversely represented a change in systemic blood volume and then in systemic vascular capacitance, and a change in mean arterial pressure directly reflected a change in systemic vascular resistance. Administration of 1% and 2% halothane produced the blood concentrations of 0.58±0.14 mM and 1.34±0.06 mM, respectively. Systemic vascular resistance decreased by 12±6% and 40±4% during 1% and 2% halothane, respecitively. Systemic blood volume increased by 7±2 ml·kg-1 and 15±4 ml·kg-1 during 1% and 2% halothane, respectively. Halothane did not cause significant blood flow redistribution between the splanchnic and extrasplanchnic vascular beds. These results suggest that halothane causes an increase in systemic vascular capacitance as well as a decrease in systemic vascular resistance. This increase in vascular capacitance may contribute in part to a decrease in cardiac output during halothane anesthesia.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system.

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

Catecholamine-induced changes in vascular capacitance and sympathetic nerve activity in dogs.

The effects of three catecholamines, dopamine, epinephrine, and dobutamine, on the systemic circulation, especially on systemic vascular capacitance, were studied using cardiopulmonary bypass in dogs anesthetized with pentobarbital. Venous outflow was divided into three compartments: splanchnic, renal, and other; changes in systemic blood volume (SBV) were calculated from the changes in total venous outflow. To examine the contribution of sympathetic discharge to these vascular responses, sympathetic efferent nerve activity (SENA) from the ventral ansa subclavian nerve was recorded simultaneously. Experiments were done under three conditions: control, after baroreceptor deafferentation, and after hexamethonium injection with low and high doses of each catecholamine. During control and after baroreceptor deafferentation, dopamine- and epinephrine-induced changes in SBV were less than those after hexamethonium, and not significant except with low dose epinephrine. After hexamethonium, dopamine (200 micrograms/kg), epinephrine (10 micrograms/kg), and dobutamine (100 micrograms/kg) reduced SBV by 10.6 +/- 3.4, 13.1 +/- 1.7, and 1.9 +/- 0.3 mL/kg, respectively. Splanchnic outflow increased significantly with dopamine and epinephrine after hexamethonium. High dose dopamine and epinephrine significantly suppressed SENA to 38 +/- 9 and 15 +/- 6% of baseline, respectively. Low dose dopamine decreased arterial pressure and SENA. This suppression in SENA was attenuated but still observed after baroreceptor deafferentation. Dobutamine reduced SBV, but had no effect on SENA. These results suggest that dopamine and epinephrine primarily decrease SBV by venoconstriction in the splanchnic region, however, these effects are greatly modified by basal sympathetic discharge and changes in SENA and vascular tone.

The influence of isoflurane on the vascular reflex response to lung inflation in dogs.

Positive pressure ventilation can affect hemodynamic stability by neuroreflex-mediated activity. Inhalational anesthesia is known to attenuate the arterial baroreflex function; however, little information is known about the effect of volatile anesthetics on the lung inflation reflex. The influence of isoflurane on static lung inflation reflex-induced changes in venous capacitance and systemic resistance was investigated in dogs. After controlling carotid sinus pressure at 50 mmHg and initiating total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10 and 20 mmHg. The systemic vascular resistance index (SVRI) decreased by 0.04 +/- 0.03 and 0.13 +/- 0.03 mmHg.kg.min.ml-1 during tracheal inflation pressures of 10 and 20 mmHg, respectively. There as an accompanying change in systemic vascular capacitance index (SVCI) by 1.0 +/- 0.65 and 3.3 +/- 0.82 ml.kg-1 during tracheal inflation pressures of 10 and 20 mmHg. The addition of isoflurane decreased the reflex vascular response to lung inflation in a dose-dependent manner. A concentration of 1 MAC isoflurane administered via the cardiopulmonary bypass machine attenuated the change in SVRI to tracheal inflation pressures of 10 and 20 mmHg by 75% and 67%, respectively. Isoflurane at 1 MAC also reduced the reflex capacitance response to tracheal pressures of 10 and 20 mmHg by 36% each. Lung inflation-induced changes in SVRI and SVCI were abolished at isoflurane concentrations of 2 MAC. We conclude that under the conditions of this study, 1 MAC isoflurane was shown to attenuate lung reflex-induced changes in SVRI and SVCI and that at higher isoflurane concentrations (2 MAC) these reflex-induced changes were not seen.

Modifications by Halothane of Responses to Acute Hypoxia in Systemic Vascular Capacitance, Resistance, and Sympathetic Nerve Activity in Dogs

To examine the effects of halothane on segmental vascular responses to hypoxia, we used cardiopulmonary bypass with venous outflow divided into three compartments (splanchnic, coronary, and "other") in dogs anesthetized with pentobarbital sodium. The reservoir volume changes represented the inverted changes in systemic blood volume (SBV). In addition, sympathetic efferent nerve activity (SENA) was simultaneously recorded from the ventral ansa subclavian nerve. Experiments were done in two groups: severe hypoxia (PO2 of 19 mm Hg) and moderate hypoxia (PO2 of 50 mm Hg). Hypoxia provoked a significant decrease in SBV of 22.3 +/- 3.1 mL/kg and 10.5 +/- 1.6 mL/kg during severe and moderate hypoxia, respectively. Two percent end-tidal halothane attenuated the decrease in SBV to 10.3 +/- 1.3 mL/kg during severe hypoxia, and 1% halothane attenuated the decrease to 3.7 +/- 1.4 mL/kg during moderate hypoxia. Subsequent chemoreceptor denervation in the presence of 1% halothane completely abolished the moderate hypoxia-induced decrease in SBV. In the presence of halothane, vascular resistance during hypoxia was significantly less than that during control conditions. Sympathetic efferent nerve activity increased significantly during severe and moderate hypoxia by about 180% and 55%, respectively. During severe hypoxia, halothane did not cause any change in the response of SENA, whereas during moderate hypoxia, halothane tended to decrease SENA, but not significantly, and subsequent chemoreceptor denervation completely abolished the increase in SENA. Coronary resistance showed a hypoxia-induced reduction that was not influenced by halothane. These results suggest that acute hypoxia causes a decrease in SBV dependent on the severity of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of lung inflation reflex on vascular capacitance in the systemic circulation

The effects of sustained lung inflation on systemic vascular capacitance (SVC), systemic vascular resistance (SVR), and cardiac sympathetic efferent nerve activity (SENA) were investigated in anesthetized dogs. By use of a total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10, 15, and 20 mmHg. Tracheal pressures of 10, 15, and 20 mmHg increased system vascular capacitance by 1.4, 3.1, and 4.3 ml/kg and decreased systemic vascular resistance by 0.11, 0.15, and 0.16 mmHg.kg.min-ml-1, respectively, at low carotid sinus pressure (CSP) of 41 mmHg. SENA showed a concomitant decrease. Bilateral vagotomy attenuated the change in SVR by 69%, SVC by 62%, and SENA by 97% when lungs were inflated to a tracheal pressure of 20 mmHg at a low CSP. These results indicate that lung inflation causes a reflex induced increase in SVC as well as a decrease in both SVR and SENA. The lung inflation reflex is mediated primarily through vagal afferent nerve fibers with a small contribution from other afferent nerve pathways.

Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog.

The role of alpha 2-adrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct alpha 2-adrenergic receptor agonists, UK 14,304 and B-HT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 micrograms/min) resulted in increased arterial resistance (mean arterial pressure increased 18 +/- 4 [SEM] mm Hg; p less than 0.01) and a decrease in systemic vascular capacity (81 +/- 20 ml; p less than 0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 theta grams/min) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for beta 2-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact animal would increase venous return to the heart.

Left ventricular reflex control of venous return and systemic vascular capacitance in dogs.

The reflex effects of left ventricular distension on venous return, vascular capacitance, vascular resistance, and sympathetic efferent nerve activity were examined in dogs anesthetized with sodium pentobarbital. In addition, the interaction of left ventricular distension and the carotid sinus baroreflex was examined. Vascular capacitance was assessed by measuring changes in systemic blood volume, using extracorporeal circulation with constant cardiac output and constant central venous pressure. Left ventricular distension produced by balloon inflation caused a transient biphasic change in venous return; an initial small increase was followed by a late relatively large decrease. Left ventricular distension increased systemic blood volume by 3.8 +/- 0.6 mL/kg and decreased systemic blood pressure by 27 +/- 2 mmHg (1 mmHg = 133.3 Pa) at an isolated carotid sinus pressure of 50 mmHg. These changes were accompanied by a simultaneous decrease in sympathetic efferent nerve activity. When the carotid sinus pressure was increased to 125 and 200 mmHg, these responses were attenuated. It is suggested that left ventricular mechanoreceptors and carotid baroreceptors contribute importantly to the control of venous return and vascular capacitance.

Aortic arch reflex control of total systemic vascular capacity.

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Changes in canine cardiac function and venous return curves by the carotid baroreflex.

Venous return curves and cardiac function relationships were simultaneously determined in 10 pentobarbital-anesthetized dogs at three different isolated carotid sinus pressures. Changing carotid sinus pressure (CSP) between 50 and 200 mmHg produced large changes in the zero flow intercept of the venous return curves from 15.37 +/- 0.97 to 11.94 +/- 1.36 mmHg (P less than 0.001) but no change in slope. These changes in the intercept of the venous return curve were due to alterations in systemic vascular capacity caused by the carotid sinus baroreceptor reflex. Changes in the cardiac function curve with baroreceptor pressure were masked by concomitant changes in arterial pressure afterload; however, when arterial pressure was controlled, there was a significant change in the slope of the cardiac function curve from 60.32 +/- 26.9 to 37.06 +/- 13.31 ml X min-1 X kg-1 X mmHg-1 as CSP was changed from 50 to 200 mmHg. We conclude that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output during activation of the carotid sinus baroreflex.

Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs.

The magnitude of vascular capacitance change induced by hypercapnia, hypoxia, or hypoxic hypercapnia was estimated during the administration of experimental gas mixtures to anesthetized dogs for 25 min. Mean circulatory filling pressure (Pcf) was determined by fibrillating the heart and equilibrating arterial and venous pressures with a pump. We assumed that the total blood volume remained constant and that the magnitude of change in peripheral venous volume equaled the sum of the changes in blood volume in the cardiopulmonary and arterial beds. We further assumed that active (reflex) peripheral venoconstriction occurred if the cardiopulmonary and arterial bed blood volumes, as well as the Pcf, increased. Within 3 min, severe hypercapnia and hypoxic hypercapnia induced a 5.2 and 7.3 ml/kg reduction in systemic vascular capacity, and, by 19 min of experimental gas presentation, increased Pcf by 5.5 and 7.0 mmHg, respectively. Severe hypoxia had less effect (0.7 ml/ kg and 2.5 mmHg, respectively) at 19 min. Severe hypercapnia also increased the central venous, systemic arterial, and pulmonary arterial pressures and decreased heart rate. Hypoxic hypercapnia additionally increased cardiac output. We conclude that severe systemic hypercapnia, whether alone or in combination with hypoxia, causes a significant active reduction in vascular capacitance, but severe hypoxia is less effective.

Effect of dobutamine on systemic capacity in the dog.

Dobutamine, a recently synthesized catecholamine, was developed as an agent which would produce increased inotropy in low cardiac output states without major changes in heart rate, cardiac rhythm, or peripheral vascular resistance. However, the effect of dobutamine on the capacitance vasculature is unknown. Since alterations of systemic vascular capacity influence venous return and hence cardiac output, we performed the present study. The muscular capsules of the canine spleen make them representative of the capacitance vasculature. We weighed exteriorized canine spleens continuously in 26 anesthetized dogs. Dobutamine infused for 15 minutes at 4 and 16 /ig/kg per min was associated with decreases in splenic weight of 15 ± 2% (SEM) (P < 0.0005) and 33 ± 2% (P < 0.0001) from controls of 249 ± 27 g and 313 ± 42 g. Dobutamine-induced splenic contraction was abolished by phenoxybenzamine but not by propranolol. Injections of dobutamine into the splenic artery produced significant decreases in splenic weight without any change in systemic hemodynamics. In six additional dogs with ganglionic blockade and supported by total cardiopulmonary bypass, decreases or increases in vascular volume were recorded as changes in oxygenator volume. Dobutamine infusion at 30 pg/kg per min for 10 to 24 minutes in these dogs was associated with decreases in vascular volume of 259 ± 28 ml (P < 0.0001). Selective blockade revealed the dobutamine effect to be mediated by a-adrenergic receptor stimulation alone. Thus, in the intact animal, the administration of dobutamine should increase venous return and hence cardiac output through an a-adrenergic-mediated decrease in systemic vascular capacity. Circ Res 46:133-138, 1980

Control of Total Systemic Vascular Capacity by the Carotid Sinus Baroreceptor Reflex

To attain a quantitative understanding of carotid sinus baroreceptor reflex control of cardiac output, we studied the reflex control of total systemic vascular capacity in vagotomized dogs. In experiments measuring blood volume shifts caused by the carotid sinus reflex (series 1), venous return was diverted into a reservoir while cardiac output and central venous pressure were maintained at constant levels. The pressure in the isolated carotid sinuses (ISP) was lowered or raised in 25-mm Hg steps between 75 and 200 mm Hg. This procedure mobilized blood into or out of the reservoir, indicating a decrease or an increase in total vascular capacity, respectively. The mean maximum volume shift, 3.6 ml/kg body weight, occurred in the same ISP region, 135 ± 12.5 mm Hg, where reflex control of total peripheral resistance was strongest. The total volume shift was approximately 7.5 ml/kg for ISP changes from 75 to 200 mm Hg. When mean arterial blood pressure was maintained constant during the ISP step changes, the volume shift almost doubled. In experiments measuring the reflex effect on total systemic vascular compliance (series 2) and in experiments determining the reflex control of arterial compliance (series 3), total systemic vascular and lumped arterial compliances were measured in the same dogs that were used in series 1 experiments. The total systemic vascular and arterial compliances were approximately 2.0 ml/mm Hg kg -1 and 0.0677 ml/mm Hg kg -1 , respectively. The reflex did not affect these compliances. We concluded that the reflex controls the total systemic venous capacity to a degree that changes cardiac output potentially by 30-10% per 25-mm Hg change in ISP.

Comparison of effects of angiotensin and norepinephrine on pulmonary circulation, systemic arteries and veins, and systemic vascular capacity in the dog.

In dog experiments, angiotensin II and norepinephrine were compared in regard to some components of the generalized pressor response each of these agents produces. It was found that angiotensin II has no direct effect on pulmonary blood vessels, in contrast to the pulmonary vasoconstrictor effect of norepinephrine. Angiotensin II appeared to have no effects on veins or the systemic vascular capacity, while norepinephrine was a potent venoconstrictor with, therefore, a marked ability to reduce the systemic vascular capacity.

A method for the study of the circulation in the dog using a mechanical left ventricle.

SPECIAL COMMUNICATIONSA Method for the Study of the Circulation in the Dog Using a Mechanical Left VentricleJohn C. Rose, Herbert P. Broida, Charles A. Hufnagel, John F. Gillespie, Pierre J. Rabile, and Edward D. FreisJohn C. Rose, Herbert P. Broida, Charles A. Hufnagel, John F. Gillespie, Pierre J. Rabile, and Edward D. FreisPublished Online:01 Mar 1955https://doi.org/10.1152/jappl.1955.7.5.580MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Download PDF FiguresReferencesRelatedInformationCited ByMechanical simulation of cardiac function by means of pulsatile blood pumpsJournal of Cardiothoracic and Vascular Anesthesia, Vol. 11, No. 3Cardiovascular responses to PGI2 (prostacyclin) in the dog.Circulation Research, Vol. 42, No. 2Systemic Blood Pressure Response to Changes in Right Ventricular FunctionCirculation Research, Vol. 14, No. 5Comparison of Effects of Angiotensin and Norepinephrine on Pulmonary Circulation, Systemic Arteries and Veins, and Systemic Vascular Capacity in the DogCirculation, Vol. 25, No. 1The sympathetic nervous system, the vascular volume and the venous return in relation to cardiovascular integrationThe American Journal of Medicine, Vol. 22, No. 2 More from this issue > Volume 7Issue 5March 1955Pages 580-584 https://doi.org/10.1152/jappl.1955.7.5.580PubMed14367248History Published online 1 March 1955 Published in print 1 March 1955 Metrics

Venous Return as Affected by Cardiac Output and Total Peripheral Resistance

Venous Return as Affected by Cardiac Output and Total Peripheral Resistance