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Hepatic circulation

Clive V. Greenway, W. Wayne Lautt

10.1002/cphy.cp060141

Source: Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Anatomy and Microcirculation
1.1 Origin and Distribution of Hepatic Blood Supply
1.2 Microcirculation
2 Blood Flows and Vascular Resistance
2.1 Sinusoidal Pressure
2.2 Relation Between Portal Flow and Liver Mass
2.3 Intrinsic Hepatic Arterial Flow Regulation
2.4 Extrinsic Hepatic Arterial Flow Regulation
3 Effects of Hepatic Blood Flow On Uptake of Substrates
3.1 Goresky Model
3.2 Equilibrium Model
3.3 Parallel‐Tube Model
3.4 Comparison of Models
3.5 Measurement of Hepatic Blood Flow by Uptake
4 Hepatic Blood Volume
4.1 Basic Principles, Terminology, and Normal Values
4.2 Hepatic Blood Volume in Perspective
4.3 Passive Changes in Hepatic Blood Volume
4.4 Active Capacitance Vessel Constriction
4.5 Reflex Control of Hepatic Venous Bed
4.6 Control of Cardiac Preload and Responses to Drugs
4.7 Other Complex Responses Involving Hepatic Venous Bed
4.8 Future Prospects
4.9 Hepatic Fluid Exchange
4.10 Sites of Filtration and Interstitial Fluid
4.11 Reabsorption of Filtered Fluid
4.12 Effects of Drugs on Fluid Exchange
4.13 Effects of Hepatic Nerve Stimulation on Fluid Exchange
Figure 1. Figure 1.

Diagram of hepatic vascular bed.
Figure 2. Figure 2.

Hepatic venous pressure profiles in basal state and at stable plateau phase during stimulation of hepatic nerves in cats. Portal venous pressure (PVP) and central venous pressure (CVP) were measured from stationary cannulas, whereas lobar venous profile was obtained by progressive withdrawal of lobar catheter. Pressures in portal vein and deep lobar venous pressures were not significantly different. Because pooled curves conceal steep contour of individual curves, data are recalculated in Fig. 3.

From Lautt et al. 232
Figure 3. Figure 3.

Hepatic venous pressure profiles recalculated from Fig. 2. Steepest portion of each profile curve was identified (RO), and pressure drop proximal and distal to this position was calculated. Most postsinusoidal resistance occurs across a short segment of veins, and hepatic nerves cause constriction at this same site. Pressure gradient from portal vein (PV) to 5 mm proximal to hepatic venous sphincter is on left and pressure gradient between a site 10 mm distal to sphincter and inferior vena cava (IVC) is on right.

From Lautt et al. 232
Figure 4. Figure 4.

Junctions of hepatic arterioles, portal venules, and sinusoids in the space of Mall showing postulated site of adenosine production. This adenosine concentration, which determines hepatic arteriolar tone, is regulated by production and washout into portal and hepatic arterial blood.

From Lautt et al. 235
Figure 5. Figure 5.

Arterial pressure, portal pressure, and hepatic arterial flow responses to stimulation of hepatic nerves in 1 cat and 1 dog. Note occurrence of autoregulatory escape of flow response in cat but not in dog.

From Greenway and Oshiro 130
Figure 6. Figure 6.

Left panel: relationship between liver blood flow and total hepatic clearance for drugs with various extraction rates. Arrows, normal physiological range of liver blood flow in humans; extraction values (E.R.) refer to normal flow of 1.5 liters/min. Right panel: relationship between extraction and liver blood flow for drugs with varying extraction values at a normal flow of 1.5 liters/min.

From Wilkinson and Shand 380
Figure 7. Figure 7.

Pressure‐volume relationship in hepatic venous bed (solid line). At transmural pressure P, hepatic blood volume or capacitance is C, [unstressed volume (U) plus stressed volume]. Slope of solid line, compliance. Venoconstriction (arrow) could result from a change in compliance with no change in unstressed volume (line 1), a change in unstressed volume with no change in compliance (line 2), or a combination of changes in both compliance and unstressed volume.
Figure 8. Figure 8.

Relationships between hepatic blood volume and intrahepatic pressure before, during, and after infusion of norepinephrine (NE), determined by varying portal flow (left panel) or by varying hepatic outflow pressure (right panel). Values are means ± SE; n = 9 for cats.

From Greenway et al. 134
Figure 9. Figure 9.

Effects of hepatic nerve stimulation on hepatic volume recorded by plethysmography in 1 dog.

From Greenway and Oshiro 130
Figure 10. Figure 10.

Mean (±; SE) changes in hepatic volume during hepatic nerve stimulation in 13 dogs and 15 cats. Mean control hepatic blood volume was 31 ml/100 g liver in dogs and 27 ml/100 g liver in cats.

From Greenway and Oshiro 130
Figure 11. Figure 11.

Frequency‐response curves for capacitance and resistance responses to hepatic nerve stimulation in cats.

From Green‐way et al. 137
Figure 12. Figure 12.

Effects of hepatic nerve stimulation in 1 cat before and after hemorrhage. Note that in spite of the change in stressed volume after hemorrhage, change in unstressed volume produced by nerve stimulation is almost unchanged. Thus effects of passive and active mobilization of blood volume are additive.
Figure 13. Figure 13.

Increases and decreases in splanchnic blood volume and flow in response to graded isolated changes in pressure in carotid sinus in 5 dogs. Points indicate response to increase or decrease in carotid sinus pressure from constant (windkessel‐controlled) systemic arterial pressure. Control pressure for each dog is listed.

From Brooksby and Donald 41
Figure 14. Figure 14.

Effects of intravenous epinephrine infusions on cardiac output and other variables in 10 cats (left panel) and effects of epinephrine predicted by computer model (right panel). Venous capacitance for cats is hepatic in ml · mmHg−1· 100 g−1 liver and that for model is total splanchnic in ml · mmHg−1 kg−1 body wt. Dashed lines,predicted responses if epinephrine did not reduce splanchnic venous capacitance (cardiac preload falls, and increase in cardiac output is markedly attenuated). *, P < 0.05; **, P < 0.01.

From Greenway and Innes 117,121
Figure 15. Figure 15.

Contribution of components of splanchnic reservoir when total blood volume was changed by hemorrhage or infusion of blood in cats.

From Greenway 117
Figure 16. Figure 16.

Changes in total hepatic volume and blood volume (mean ± SE) in 5 cats when hepatic venous pressure was increased to 9.4 mmHg for 60 min. Transsinusoidal fluid filtration was calculated by subtracting mean values of two curves.

From Greenway and Lautt 123
Figure 17. Figure 17.

Filtration rates induced by 3 levels of increased hepatic venous pressure during control periods (C) and during hepatic nerve stimulation at frequencies of 2, 4, and 8 Hz in 6 cats (means ± SE; *, P < 0.05; **, P < 0.01). Control portal pressure was 6.7 mmHg.

From Greenway 113


Figure 1.

Diagram of hepatic vascular bed.



Figure 2.

Hepatic venous pressure profiles in basal state and at stable plateau phase during stimulation of hepatic nerves in cats. Portal venous pressure (PVP) and central venous pressure (CVP) were measured from stationary cannulas, whereas lobar venous profile was obtained by progressive withdrawal of lobar catheter. Pressures in portal vein and deep lobar venous pressures were not significantly different. Because pooled curves conceal steep contour of individual curves, data are recalculated in Fig. 3.

From Lautt et al. 232


Figure 3.

Hepatic venous pressure profiles recalculated from Fig. 2. Steepest portion of each profile curve was identified (RO), and pressure drop proximal and distal to this position was calculated. Most postsinusoidal resistance occurs across a short segment of veins, and hepatic nerves cause constriction at this same site. Pressure gradient from portal vein (PV) to 5 mm proximal to hepatic venous sphincter is on left and pressure gradient between a site 10 mm distal to sphincter and inferior vena cava (IVC) is on right.

From Lautt et al. 232


Figure 4.

Junctions of hepatic arterioles, portal venules, and sinusoids in the space of Mall showing postulated site of adenosine production. This adenosine concentration, which determines hepatic arteriolar tone, is regulated by production and washout into portal and hepatic arterial blood.

From Lautt et al. 235


Figure 5.

Arterial pressure, portal pressure, and hepatic arterial flow responses to stimulation of hepatic nerves in 1 cat and 1 dog. Note occurrence of autoregulatory escape of flow response in cat but not in dog.

From Greenway and Oshiro 130


Figure 6.

Left panel: relationship between liver blood flow and total hepatic clearance for drugs with various extraction rates. Arrows, normal physiological range of liver blood flow in humans; extraction values (E.R.) refer to normal flow of 1.5 liters/min. Right panel: relationship between extraction and liver blood flow for drugs with varying extraction values at a normal flow of 1.5 liters/min.

From Wilkinson and Shand 380


Figure 7.

Pressure‐volume relationship in hepatic venous bed (solid line). At transmural pressure P, hepatic blood volume or capacitance is C, [unstressed volume (U) plus stressed volume]. Slope of solid line, compliance. Venoconstriction (arrow) could result from a change in compliance with no change in unstressed volume (line 1), a change in unstressed volume with no change in compliance (line 2), or a combination of changes in both compliance and unstressed volume.



Figure 8.

Relationships between hepatic blood volume and intrahepatic pressure before, during, and after infusion of norepinephrine (NE), determined by varying portal flow (left panel) or by varying hepatic outflow pressure (right panel). Values are means ± SE; n = 9 for cats.

From Greenway et al. 134


Figure 9.

Effects of hepatic nerve stimulation on hepatic volume recorded by plethysmography in 1 dog.

From Greenway and Oshiro 130


Figure 10.

Mean (±; SE) changes in hepatic volume during hepatic nerve stimulation in 13 dogs and 15 cats. Mean control hepatic blood volume was 31 ml/100 g liver in dogs and 27 ml/100 g liver in cats.

From Greenway and Oshiro 130


Figure 11.

Frequency‐response curves for capacitance and resistance responses to hepatic nerve stimulation in cats.

From Green‐way et al. 137


Figure 12.

Effects of hepatic nerve stimulation in 1 cat before and after hemorrhage. Note that in spite of the change in stressed volume after hemorrhage, change in unstressed volume produced by nerve stimulation is almost unchanged. Thus effects of passive and active mobilization of blood volume are additive.



Figure 13.

Increases and decreases in splanchnic blood volume and flow in response to graded isolated changes in pressure in carotid sinus in 5 dogs. Points indicate response to increase or decrease in carotid sinus pressure from constant (windkessel‐controlled) systemic arterial pressure. Control pressure for each dog is listed.

From Brooksby and Donald 41


Figure 14.

Effects of intravenous epinephrine infusions on cardiac output and other variables in 10 cats (left panel) and effects of epinephrine predicted by computer model (right panel). Venous capacitance for cats is hepatic in ml · mmHg−1· 100 g−1 liver and that for model is total splanchnic in ml · mmHg−1 kg−1 body wt. Dashed lines,predicted responses if epinephrine did not reduce splanchnic venous capacitance (cardiac preload falls, and increase in cardiac output is markedly attenuated). *, P < 0.05; **, P < 0.01.

From Greenway and Innes 117,121


Figure 15.

Contribution of components of splanchnic reservoir when total blood volume was changed by hemorrhage or infusion of blood in cats.

From Greenway 117


Figure 16.

Changes in total hepatic volume and blood volume (mean ± SE) in 5 cats when hepatic venous pressure was increased to 9.4 mmHg for 60 min. Transsinusoidal fluid filtration was calculated by subtracting mean values of two curves.

From Greenway and Lautt 123


Figure 17.

Filtration rates induced by 3 levels of increased hepatic venous pressure during control periods (C) and during hepatic nerve stimulation at frequencies of 2, 4, and 8 Hz in 6 cats (means ± SE; *, P < 0.05; **, P < 0.01). Control portal pressure was 6.7 mmHg.

From Greenway 113
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Article Title: Hepatic circulation
 

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Clive V. Greenway, W. Wayne Lautt. Hepatic circulation. Compr Physiol 2011, Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation: 1519-1564. First published in print 1989. doi: 10.1002/cphy.cp060141