Lymphatic function in the liver after hepatic venous pressure elevation

Elk, J. R.; Drake, R. E.; Williams, J. Powell; Gabel, J. C.; Laine, Glen A.

doi:10.1152/ajpgi.1988.254.5.g748

Cited by 9 publications

(11 citation statements)

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“…Within the interstitium, following Elk et al (1988), we assume that lymph uptake follows a linear relationshipwhere is the conductance of the lymphatic vessels and is the pressure within the flowing lymph; negative uptake is not possible, due to the presence of valves. See also the papers by Stewart and Laine (2001) and by Quick et al (2008), and Appendix 6.4.…”

Section: Mathematical Modelmentioning

confidence: 99%

“…Elk et al (1988) performed experiments on anesthetized dogs weighing 20–30 kg to determine the flow rate into the lymphatic vessels as a function of interstitial pressure. They found that the volumetric flux of lymph leaving the liver equaled , where O min/ is the resistance of the ducts.…”

Section: Appendix A: Analytical Modelmentioning

confidence: 99%

“…There are lymphatic vessels distributed throughout the lobule, and these take up interstitial fluid actively at a regulated rate; however, the dependence of the rate of uptake upon the interstitial pressure and other parameters is not fully known. Elk et al (1988) performed experiments on livers of anesthetized dogs to determine typical rates of uptake by the lymphatic vessels. In their experiments, they determined the effective resistance of the lymphatic vessels, that is, the increase in interstitial pressure required to produce a unit increase in volumetric flux taken up by the lymphatics.…”

Section: Introductionmentioning

confidence: 99%

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Mathematical model of blood and interstitial flow and lymph production in the liver

Siggers

Leungchavaphongse

et al. 2013

Biomech Model Mechanobiol

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We present a mathematical model of blood and interstitial flow in the liver. The liver is treated as a lattice of hexagonal ‘classic’ lobules, which are assumed to be long enough that end effects may be neglected and a two-dimensional problem considered. Since sinusoids and lymphatic vessels are numerous and small compared to the lobule, we use a homogenized approach, describing the sinusoidal and interstitial spaces as porous media. We model plasma filtration from sinusoids to the interstitium, lymph uptake by lymphatic ducts, and lymph outflow from the liver surface. Our results show that the effect of the liver surface only penetrates a depth of a few lobules’ thickness into the tissue. Thus, we separately consider a single lobule lying sufficiently far from all external boundaries that we may regard it as being in an infinite lattice, and also a model of the region near the liver surface. The model predicts that slightly more lymph is produced by interstitial fluid flowing through the liver surface than that taken up by the lymphatic vessels in the liver and that the non-peritonealized region of the surface of the liver results in the total lymph production (uptake by lymphatics plus fluid crossing surface) being about 5 % more than if the entire surface were covered by the Glisson–peritoneal membrane. Estimates of lymph outflow through the surface of the liver are in good agreement with experimental data. We also study the effect of non-physiological values of the controlling parameters, particularly focusing on the conditions of portal hypertension and ascites. To our knowledge, this is the first attempt to model lymph production in the liver. The model provides clinically relevant information about lymph outflow pathways and predicts the systemic response to pathological variations.

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Section: Mathematical Modelmentioning

confidence: 99%

Section: Appendix A: Analytical Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mathematical model of blood and interstitial flow and lymph production in the liver

Siggers

Leungchavaphongse

et al. 2013

Biomech Model Mechanobiol

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“…They are therefore empirical (descriptive) parameters (15). To date, R L and P p have been used to describe lymphatic function in a number of organs (16,18,20,43,45) but have yet to be assigned particular physiological interpretations. Much like K f , a black box parameter relating hydrostatic and colloid osmotic pressure gradients to microvascular filtration and C, a black box parameter relating interstitial fluid R655 EDEMAGENIC GAIN AJP-Regul Integr Comp Physiol • VOL 294 • FEBRUARY 2008 • www.ajpregu.org volume to pressure, R L and P p are similar black box parameters, which relate lymphatic outflow to interstitial fluid pressure.…”

Section: Discussionmentioning

confidence: 99%

Edemagenic gain and interstitial fluid volume regulation

Dongaonkar

Quick²,

Stewart³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Under physiological conditions, interstitial fluid volume is tightly regulated by balancing microvascular filtration and lymphatic return to the central venous circulation. Even though microvascular filtration and lymphatic return are governed by conservation of mass, their interaction can result in exceedingly complex behavior. Without making simplifying assumptions, investigators must solve the fluid balance equations numerically, which limits the generality of the results. We thus made critical simplifying assumptions to develop a simple solution to the standard fluid balance equations that is expressed as an algebraic formula. Using a classical approach to describe systems with negative feedback, we formulated our solution as a "gain" relating the change in interstitial fluid volume to a change in effective microvascular driving pressure. The resulting "edemagenic gain" is a function of microvascular filtration coefficient (K(f)), effective lymphatic resistance (R(L)), and interstitial compliance (C). This formulation suggests two types of gain: "multivariate" dependent on C, R(L), and K(f), and "compliance-dominated" approximately equal to C. The latter forms a basis of a novel method to estimate C without measuring interstitial fluid pressure. Data from ovine experiments illustrate how edemagenic gain is altered with pulmonary edema induced by venous hypertension, histamine, and endotoxin. Reformulation of the classical equations governing fluid balance in terms of edemagenic gain thus yields new insight into the factors affecting an organ's susceptibility to edema.

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“…Inflation was continued until a stable portal pressure of 17.5 mm Hg was observed. This venous hypertension in both the liver and intestines resulted in increased microvascular pressures, increased microvascular filtration, increased interstitial fluid volume and pressure, and increased lymph flow from both organs (6,7,15). The pressure within the cisterna chyli was monitored until it increased to a stable value.…”

Section: Rh Stewart and Ga Lainementioning

confidence: 99%

Flow in Lymphatic Networks: Interaction between Hepatic and Intestinal Lymph Vessels

STEWART¹,

LAINE²

2001

Microcirculation

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Objective: Lymph from both the liver and intestine flows into the cisterna chyli. We hypothesized that increasing liver lymph flow would increase cisterna chyli pressure and, thereby, decrease intestinal lymph flow, potentiating intestinal edema formation. Methods: Anesthetized dogs were instrumented to measure and manipulate portal vein pressure and cisterna chyli pressure. The effects of directly increasing portal pressure with and without directly increasing cisterna chyli pressure on intestinal wet-to-dry ratio and intestinal ascites formation rate were determined. Target values for portal and cisterna chyli pressures were determined following elevation of inferior vena caval pressure to levels seen in patients with obstructive caval disease. Results: Direct elevation of portal pressure (P port ) alone to 17.5 mm Hg caused a significant increase in intestinal wet-to-dry ratio (3.98 ± 0.24 vs. 3.40 ± 0.43) and the rate of ascites formation (0.36 ± 0.12 vs. 0.05 ± 0.03 mL/g dry wt/h). Simultaneous direct elevation of cisterna chyli pressure to 6.0 mm Hg and P port to 17.5 mm Hg caused further increases in intestinal wet-to-dry ratio (5.52 ± 1.20) and ascites formation (0.57 ± 0.11 mL/g dry wt./h). Conclusions: Inferior vena caval hypertension increases liver lymph flow that elevates cisterna chyli pressure, which inhibits intestinal lymph flow and augments intestinal edema formation. Microcirculation (2001) 8, 221-227. RH Stewart and GA Laine Lymphatic-lymphatic interaction 222 RH Stewart and GA Laine Lymphatic-lymphatic interaction 227

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Lymphatic function in the liver after hepatic venous pressure elevation

Cited by 9 publications

References 0 publications

Mathematical model of blood and interstitial flow and lymph production in the liver

Mathematical model of blood and interstitial flow and lymph production in the liver

Edemagenic gain and interstitial fluid volume regulation

Flow in Lymphatic Networks: Interaction between Hepatic and Intestinal Lymph Vessels

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