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Venous System: Physiology of the Capacitance Vessels

Carl F. Rothe

10.1002/cphy.cp020313

Source: Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow

Originally published: 1983

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Synopsis
2 Perspectives
3 Definitions and Basic Concepts
3.1 Definitions
3.2 Active Contraction of Veins
3.3 Effect of Flow on Vascular Volume
3.4 Central Venous Pressure
3.5 Mean Circulatory Filling Pressure
3.6 Venous Hemodynamics
3.7 Venous Resistance
4 Structural Characteristics of Veins
4.1 Anatomy
4.2 Volume of Blood
4.3 Vascular Compliance
4.4 Linearity of Pressure‐Volume Relationship
5 Venous Return and Potential Role of Veins in Cardiovascular Homeostasis
5.1 Guytonian Relationship Between Venous Return and Cardiac Output
5.2 De Jager‐Krogh Phenomenon
5.3 Venous Pooling on Standing
6 Reflex Control of Capacitance System
6.1 Effect of Neural and Hormonal Stimulation
6.2 Baroreceptors
6.3 Chemoreceptors
6.4 Atrial, Ventricular, and Pulmonary Receptors
6.5 Receptor Interaction
6.6 Venous Myogenic Activity
6.7 Venoarteriolar Reflex
6.8 Effect of Temperature
6.9 Time Course of Reflex Response
6.10 Capacitance‐Vessel Tone
7 Veins in Health and Disease
7.1 Exercise
7.2 Vasovagal Syncope
7.3 Orthostatic Hypotension
7.4 Shock
7.5 Hypertension
8 Methods of Measurement of Vascular Capacitance
8.1 Transmural Pressure of Capacitance Vessels
8.2 Volume of Capacitance Vessels
8.3 Measures of Total‐Body Vascular Compliance and Capacitance
8.4 General Problems
9 Pharmacology of Veins
9.1 Anesthetics
9.2 Angiotensin
9.3 Catecholamines
9.4 Histamine
9.5 Morphine
9.6 Nitroprusside
9.7 Serotonin
9.8 Vasopressin
10 Future Research
Figure 1. Figure 1.

Three‐dimensional plot of average interrelationships determined simultaneously among mean right atrial pressure (MRAP), mean aortic pressure (MAP), and aortic flow (AF). Inhibition of sympathetic outflow by carotid and aortic baroreceptors blocked.

From Herndon and Sagawa 238
Figure 2. Figure 2.

Effects of volume loading with blood (right of center) compared with volume depletion (left of center) on responses of cardiac output (circles and solid lines), heart rate (triangles and dotted lines), and stroke volume (squares and dashed lines). Heart rate rose almost equally with volume loading and depletion. In contrast, stroke volume fell strikingly with hemorrhage but remained essentially constant with infusion of blood.

From Vatner and Boettcher 507, by permission of the American Heart Association, Inc
Figure 3. Figure 3.

Vascular capacitance as the relation of transmural pressure to contained volume. A, control pressure‐volume relationship. Unstressed volume is volume, estimated by extrapolation, of vessel if transmural pressure is zero; B, reduction in unstressed volume; C, reduction in compliance (increased stiffness of vasculature). With large untethered vessels there tends to be a relatively wide range of volume change with little change of transmural pressure at zero pressure because cross section of vessel changes (α). With vessels embedded in tissue, transmural pressure at volumes less than unstressed volume may be markedly negative (β).
Figure 4. Figure 4.

Volume in collapsible tube as function of transmural pressure. Typical transverse cross sections shown at various points in curve.

From Katz et al. 282
Figure 5. Figure 5.

Diameter‐pressure relationship in unexposed femoral vein before and after norepinephrine infusion in dog. (Norepinephrine administered via iv drip in cephalic vein at rate sufficient to increase mean arterial pressure 20 mmHg.)

From Morris et al. 372
Figure 6. Figure 6.

Volume contained in isolated canine saphenal vein segment at various hydrostatic pressures. Data at rest and at maximum contraction induced by constant electrical stimulation (10 s, 15/s), imposed after 2‐min stabilization against each increase in hydrostatic pressure (2 cmH2O every 5 min). •, Data at rest; ×, data during stimulation.

From Vanhoutte and Leusen 504
Figure 7. Figure 7.

Conceptual representation of technique for distinguishing between active and passive factors in change in vascular capacitance. Left panel: during electrical stimulation venous outflow transiently increased, arterial flow decreased. Integrated difference between two curves was 112 ml. Middle panel: effect of partial mechanical occlusion to decrease arterial flow to about same level as during stimulation. Both inflow and outflow decreased, giving integrated difference due to passive emptying of 55 ml. Right panel: difference of 57 ml between these two volumes, or integrated difference between two venous outflow curves assuming equal arterial flow patterns, represents active component.

From Shepherd 462, copyright © 1978 by Year Book Medical Publishers, Inc., Chicago
Figure 8. Figure 8.

Flow effect on changes in total hepatic blood volume (ΔV) at different levels of changes from control of total hepatic inflow (Fin). Symbols, flow changed via hepatic artery; lines, flow changed via portal vein inflow.

From Bennett and Rothe 37
Figure 9. Figure 9.

Diagram of blood vessel pattern in vein walls.

From O'Neill 388
Figure 10. Figure 10.

Diagrammatic representation of relationship between adrenergic nerves and mesenteric blood vessels: pa, principal artery; pv, principal vein; sa, small artery of microvasculature; ta, terminal arteriole; pca, precapillary arteriole; c, capillary; cv, collecting venule; sv, small vein. Adrenergic nerves represented by heavy lines. Arrows indicate direction of blood flow. Note that precapillary arterioles and collecting venules are not innervated.

From Furness and Marshall 154
Figure 11. Figure 11.

Average changes in venous pressure at ankle produced by walking 1.7 mph.

From Pollack and Wood 404
Figure 12. Figure 12.

Total‐body pressure‐volume relationship of chloralose‐anesthetized dogs. Upper panel: mean circulatory pressure (Pmc) of control group after various changes in blood volume as function of time after changing volume. Compensatory mechanisms tend to restore mean circulatory filling pressure after various volume changes shown. Lower panel: mean circulatory pressure changes as function of blood volume at 0.5 min after start of volume change at control and after sympathetic ganglionic blocking agent, hexamethonium. Mean circulatory filling pressure (Pmc) is linearly related to change in blood volume in range of about 5–25 mmHg.

From Drees and Rothe 125, by permission of the American Heart Association, Inc
Figure 13. Figure 13.

Cardiac output curves for normal heart, for hyper‐ and hypoeffective hearts, and for hearts subjected to increased or decreased resistive loads, that is, increased or decreased arterial pressures.

From Guyton 208
Figure 14. Figure 14.

Effect on venous return curve caused by changes in mean systemic filling pressure (Pms).

From Guyton 208
Figure 15. Figure 15.

Equilibrium right atrial pressure of venous return and cardiac output curves under various conditions: A, normal; B, damaged myocardium with compensatory increase in mean circulatory filling pressure (MCFP); C, sympathetic stimulation of heart and periphery, such as in exercise with equilibrium right atrial pressure not changed from normal; D, increased right atrial pressure with no change in cardiac function; venous return curve increased by increase in blood volume or venoconstriction causing increased mean circulatory filling pressure; E, reduced right atrial pressure with sympathetic enhancement of cardiac function during hemorrhage; F, equilibrium with damaged heart and reduced blood volume, such as in uncompensated irreversible hemorrhage in shock; right atrial pressure normal.

Adapted from Guyton 207
Figure 16. Figure 16.

Mean changes in hepatic blood volume during hepatic nerve stimulation. Mean hepatic blood volume at control was 31 ml/100 g liver in dogs and 27 ml/100 g in cats.

From Greenway and Oshiro 192
Figure 17. Figure 17.

Steady‐state changes in reservoir volume versus carotid intrasinus pressure. Volume changes corrected to that intrasinus pressure giving the maximal response (ISP0).

From Shoukas and Sagawa 468, by permission of the American Heart Association, Inc
Figure 18. Figure 18.

Total‐body pressure‐volume relationship in dogs. Mean circulatory pressure (Pmc) at various blood volumes with ganglionic blockade (relaxed) or maximal stimulation by norepinephrine (constricted) compared with control 5 min after blood volume change. Chloralose anesthesia. Spleen intact. Confidence bands at 5% level shown. Control blood volume for areflexic group after 8.5 ml/kg transfusion.

From Drees and Rothe 125, by permission of the American Heart Association, Inc
Figure 19. Figure 19.

Stimulus‐response curves showing simultaneous changes in arterial blood pressure, liver blood volume, total hepatic blood flow, and hepatic arterial and portal venous resistances during step changes in carotid sinus pressure from a control level of 169 mmHg. Anesthetized dog with vagi cut. Changes calculated as % of control values. HAF, hepatic arterial flow; PVF, portal venous flow; HAR, hepatic arterial resistance; PVR, portal venous resistance.

From Carneiro and Donald 77, by permission of the American Heart Association, Inc
Figure 20. Figure 20.

Three‐dimensional plot of vascular pressure‐to‐volume relationship in dogs. A: volume trajectory hypothesized during instantaneous reduction in volume of about 17 ml/kg body weight to bring mean circulatory filling pressure (Pmc) to 4 mmHg and volume change then required to maintain this Pmc. B: changes of mean circulatory pressure with time after reduction in blood volume of 17 ml/kg. C: pressure‐volume relationship during cardiac fibrillation for 1 min. Mean circulatory filling pressure returned to and held at control value by removing volume from animal starting at about 15 s.

Adapted from Rothe 432, by permission of the American Heart Association, Inc.; data in curve B from Drees and Rothe 125
Figure 21. Figure 21.

Different patterns of cardiac and resistant vessel responses resulting from different types of chemoreceptor stimulation. Top, arterial hypoxia; middle, carbon monoxide hypoxia; bottom, hemorrhage of 6% of animal's blood volume plus its increased heart rate or vasoconstriction; black, average neuro source of effector stimulation; striped, adrenal catecholamine; open, local.

From Korner 288
Figure 22. Figure 22.

Process of obtaining mean transit time () of indicator.
Figure 23. Figure 23.

Basic concepts for determining mean transit time () using indicator dilution.

Adapted from Lassen and Perl 305
Figure 24. Figure 24.

Diagrammatic representation of technique of estimating changes in vascular capacitance. A: reservoir approach. Constant flow perfusion of right heart and return of all venous blood to reservoir at fixed venous pressure (Pv). Compliance estimated as ratio of volume change to step change in Pv. B: technique using closed system. Compliance estimated as change in central venous pressure (Pv) in response to known change of injected volume (ΔV).

From Rothe 434
Figure 25. Figure 25.

Mean circulatory pressure technique. Blood volume reduced by rapid hemorrhage 0.5 min before. Heart fibrillated, blood pumped from aorta to vena cava until pressures equal. PA, arterial pressure; PCV, raw central venous pressure; , averaged and expanded central venous pressure; PMC, mean circulatory filling pressure at equilibrium obtained before 7 s after start of arterial pressure decrease; ΔPA‐V, difference between aortic and central venous pressures.

From Drees and Rothe 125, by permission of the American Heart Association, Inc


Figure 1.

Three‐dimensional plot of average interrelationships determined simultaneously among mean right atrial pressure (MRAP), mean aortic pressure (MAP), and aortic flow (AF). Inhibition of sympathetic outflow by carotid and aortic baroreceptors blocked.

From Herndon and Sagawa 238


Figure 2.

Effects of volume loading with blood (right of center) compared with volume depletion (left of center) on responses of cardiac output (circles and solid lines), heart rate (triangles and dotted lines), and stroke volume (squares and dashed lines). Heart rate rose almost equally with volume loading and depletion. In contrast, stroke volume fell strikingly with hemorrhage but remained essentially constant with infusion of blood.

From Vatner and Boettcher 507, by permission of the American Heart Association, Inc


Figure 3.

Vascular capacitance as the relation of transmural pressure to contained volume. A, control pressure‐volume relationship. Unstressed volume is volume, estimated by extrapolation, of vessel if transmural pressure is zero; B, reduction in unstressed volume; C, reduction in compliance (increased stiffness of vasculature). With large untethered vessels there tends to be a relatively wide range of volume change with little change of transmural pressure at zero pressure because cross section of vessel changes (α). With vessels embedded in tissue, transmural pressure at volumes less than unstressed volume may be markedly negative (β).



Figure 4.

Volume in collapsible tube as function of transmural pressure. Typical transverse cross sections shown at various points in curve.

From Katz et al. 282


Figure 5.

Diameter‐pressure relationship in unexposed femoral vein before and after norepinephrine infusion in dog. (Norepinephrine administered via iv drip in cephalic vein at rate sufficient to increase mean arterial pressure 20 mmHg.)

From Morris et al. 372


Figure 6.

Volume contained in isolated canine saphenal vein segment at various hydrostatic pressures. Data at rest and at maximum contraction induced by constant electrical stimulation (10 s, 15/s), imposed after 2‐min stabilization against each increase in hydrostatic pressure (2 cmH2O every 5 min). •, Data at rest; ×, data during stimulation.

From Vanhoutte and Leusen 504


Figure 7.

Conceptual representation of technique for distinguishing between active and passive factors in change in vascular capacitance. Left panel: during electrical stimulation venous outflow transiently increased, arterial flow decreased. Integrated difference between two curves was 112 ml. Middle panel: effect of partial mechanical occlusion to decrease arterial flow to about same level as during stimulation. Both inflow and outflow decreased, giving integrated difference due to passive emptying of 55 ml. Right panel: difference of 57 ml between these two volumes, or integrated difference between two venous outflow curves assuming equal arterial flow patterns, represents active component.

From Shepherd 462, copyright © 1978 by Year Book Medical Publishers, Inc., Chicago


Figure 8.

Flow effect on changes in total hepatic blood volume (ΔV) at different levels of changes from control of total hepatic inflow (Fin). Symbols, flow changed via hepatic artery; lines, flow changed via portal vein inflow.

From Bennett and Rothe 37


Figure 9.

Diagram of blood vessel pattern in vein walls.

From O'Neill 388


Figure 10.

Diagrammatic representation of relationship between adrenergic nerves and mesenteric blood vessels: pa, principal artery; pv, principal vein; sa, small artery of microvasculature; ta, terminal arteriole; pca, precapillary arteriole; c, capillary; cv, collecting venule; sv, small vein. Adrenergic nerves represented by heavy lines. Arrows indicate direction of blood flow. Note that precapillary arterioles and collecting venules are not innervated.

From Furness and Marshall 154


Figure 11.

Average changes in venous pressure at ankle produced by walking 1.7 mph.

From Pollack and Wood 404


Figure 12.

Total‐body pressure‐volume relationship of chloralose‐anesthetized dogs. Upper panel: mean circulatory pressure (Pmc) of control group after various changes in blood volume as function of time after changing volume. Compensatory mechanisms tend to restore mean circulatory filling pressure after various volume changes shown. Lower panel: mean circulatory pressure changes as function of blood volume at 0.5 min after start of volume change at control and after sympathetic ganglionic blocking agent, hexamethonium. Mean circulatory filling pressure (Pmc) is linearly related to change in blood volume in range of about 5–25 mmHg.

From Drees and Rothe 125, by permission of the American Heart Association, Inc


Figure 13.

Cardiac output curves for normal heart, for hyper‐ and hypoeffective hearts, and for hearts subjected to increased or decreased resistive loads, that is, increased or decreased arterial pressures.

From Guyton 208


Figure 14.

Effect on venous return curve caused by changes in mean systemic filling pressure (Pms).

From Guyton 208


Figure 15.

Equilibrium right atrial pressure of venous return and cardiac output curves under various conditions: A, normal; B, damaged myocardium with compensatory increase in mean circulatory filling pressure (MCFP); C, sympathetic stimulation of heart and periphery, such as in exercise with equilibrium right atrial pressure not changed from normal; D, increased right atrial pressure with no change in cardiac function; venous return curve increased by increase in blood volume or venoconstriction causing increased mean circulatory filling pressure; E, reduced right atrial pressure with sympathetic enhancement of cardiac function during hemorrhage; F, equilibrium with damaged heart and reduced blood volume, such as in uncompensated irreversible hemorrhage in shock; right atrial pressure normal.

Adapted from Guyton 207


Figure 16.

Mean changes in hepatic blood volume during hepatic nerve stimulation. Mean hepatic blood volume at control was 31 ml/100 g liver in dogs and 27 ml/100 g in cats.

From Greenway and Oshiro 192


Figure 17.

Steady‐state changes in reservoir volume versus carotid intrasinus pressure. Volume changes corrected to that intrasinus pressure giving the maximal response (ISP0).

From Shoukas and Sagawa 468, by permission of the American Heart Association, Inc


Figure 18.

Total‐body pressure‐volume relationship in dogs. Mean circulatory pressure (Pmc) at various blood volumes with ganglionic blockade (relaxed) or maximal stimulation by norepinephrine (constricted) compared with control 5 min after blood volume change. Chloralose anesthesia. Spleen intact. Confidence bands at 5% level shown. Control blood volume for areflexic group after 8.5 ml/kg transfusion.

From Drees and Rothe 125, by permission of the American Heart Association, Inc


Figure 19.

Stimulus‐response curves showing simultaneous changes in arterial blood pressure, liver blood volume, total hepatic blood flow, and hepatic arterial and portal venous resistances during step changes in carotid sinus pressure from a control level of 169 mmHg. Anesthetized dog with vagi cut. Changes calculated as % of control values. HAF, hepatic arterial flow; PVF, portal venous flow; HAR, hepatic arterial resistance; PVR, portal venous resistance.

From Carneiro and Donald 77, by permission of the American Heart Association, Inc


Figure 20.

Three‐dimensional plot of vascular pressure‐to‐volume relationship in dogs. A: volume trajectory hypothesized during instantaneous reduction in volume of about 17 ml/kg body weight to bring mean circulatory filling pressure (Pmc) to 4 mmHg and volume change then required to maintain this Pmc. B: changes of mean circulatory pressure with time after reduction in blood volume of 17 ml/kg. C: pressure‐volume relationship during cardiac fibrillation for 1 min. Mean circulatory filling pressure returned to and held at control value by removing volume from animal starting at about 15 s.

Adapted from Rothe 432, by permission of the American Heart Association, Inc.; data in curve B from Drees and Rothe 125


Figure 21.

Different patterns of cardiac and resistant vessel responses resulting from different types of chemoreceptor stimulation. Top, arterial hypoxia; middle, carbon monoxide hypoxia; bottom, hemorrhage of 6% of animal's blood volume plus its increased heart rate or vasoconstriction; black, average neuro source of effector stimulation; striped, adrenal catecholamine; open, local.

From Korner 288


Figure 22.

Process of obtaining mean transit time () of indicator.



Figure 23.

Basic concepts for determining mean transit time () using indicator dilution.

Adapted from Lassen and Perl 305


Figure 24.

Diagrammatic representation of technique of estimating changes in vascular capacitance. A: reservoir approach. Constant flow perfusion of right heart and return of all venous blood to reservoir at fixed venous pressure (Pv). Compliance estimated as ratio of volume change to step change in Pv. B: technique using closed system. Compliance estimated as change in central venous pressure (Pv) in response to known change of injected volume (ΔV).

From Rothe 434


Figure 25.

Mean circulatory pressure technique. Blood volume reduced by rapid hemorrhage 0.5 min before. Heart fibrillated, blood pumped from aorta to vena cava until pressures equal. PA, arterial pressure; PCV, raw central venous pressure; , averaged and expanded central venous pressure; PMC, mean circulatory filling pressure at equilibrium obtained before 7 s after start of arterial pressure decrease; ΔPA‐V, difference between aortic and central venous pressures.

From Drees and Rothe 125, by permission of the American Heart Association, Inc
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Article Title: Venous System: Physiology of the Capacitance Vessels
 

How to Cite

Carl F. Rothe. Venous System: Physiology of the Capacitance Vessels. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 397-452. First published in print 1983. doi: 10.1002/cphy.cp020313