Buffer Response Research Articles

Vegetation change at high elevation: scale dependence and interactive effects on Niwot Ridge

Background: High-elevation mountain systems may be particularly responsive to climate change.Aims: Here we investigate how changes along elevation gradients in mountain systems can aid in predicting vegetation distributional changes in time, focusing on how changing climatic controls affect meso-scale transitions at the lower and upper boundaries of alpine vegetation (with forest and subnival zones, respectively) as well as micro-scale transitions among plant communities within the alpine belt. We focus on climate-related drivers, particularly in relation to climate change, but also consider how species interactions, dispersal and responses to disturbance may influence plant responses to these abiotic drivers.Results: Empirical observations and experimental studies indicate that changing climatic controls influence both meso-scale transitions at the upper and lower boundaries of alpine vegetation and micro-scale transitions among plant communities within tundra. Micro-scale heterogeneity appears to buffer response in many cases, while interactions between climate and other changes may often accelerate change.Conclusions: Interactions with microtopography and larger edaphic gradients have the capacity to both facilitate rapid changes and reinforce stability, and that these interactions will affect the responsiveness of vegetation to climate change at different spatial scales.

Safety and efficacy of splenic artery embolization for portal hyperperfusion in liver transplant recipients: a 5-year experience.

Severe portal hyperperfusion (PHP) after liver transplantation has been shown to cause intrahepatic arterial vasoconstriction secondary to increased adenosine washout (hepatic artery buffer response). Clinically, posttransplant PHP can cause severe cases of refractory ascites and hydrothorax. In the past, we reported our preliminary experience with the use of splenic artery embolization (SAE) as a way to reduce PHP. Here we present our 5-year experience with SAE in orthotopic liver transplantation (OLT). Between January 2007 and December 2011, 681 patients underwent OLT at our institution, and 54 of these patients underwent SAE for increased hepatic arterial resistance and PHP (n=42) or refractory ascites/hepatic hydrothorax (n=12). Patients undergoing SAE were compared to a control group matched by year of embolization, calculated Model for End-Stage Liver Disease score, and liver weight. SAE resulted in improvements in hepatic artery resistive indices (0.92±0.14 and 0.76±0.10 before and after SAE, respectively; P<0.001) and improved hepatic arterial blood flow (HAF; 15.6±9.69 and 28.7±14.83, respectively; P<0.001). Calculated splenic volumes and spleen/liver volume ratios were correlated with patients requiring SAE versus matched controls (P=0.002 and P=0.001, respectively). Among the 54 patients undergoing SAE, there was 1 case of postsplenectomy syndrome. No abscesses, significant infections, or bleeding was noted. We thus conclude that SAE is a safe and effective technique able to improve HAF parameters in patients with elevated portal venous flow and its sequelae.

Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.

IntroductionThe compensatory increase in hepatic arterial flow with a decrease in portal venous flow is known as the hepatic arterial buffer response. In cirrhosis with elevated portal pressure, the vascular resistance of the hepatic artery is decreased. Whether this lower resistance of the hepatic artery is a consequence of portal hypertension or not remains unknown.Study AimThe aim of the study was to investigate the hepatic arterial resistance and response to vasoconstriction in cirrhosis without portal hypertension (normal portal resistance).MethodsCirrhosis was induced by CCl4-inhalation for 8 weeks (8W, normal portal resistance) and for 12–14 weeks (12W, elevated portal resistance). Bivascular liver perfusion was performed at 8W or 12W and dose response curves of methoxamine were obtained in the presence or absence of LNMMA (nitric oxide synthase blocker). Vascular resistances of the hepatic artery (HAR), portal vein (PVR) and sinusoids (SVR) were measured. Western Blot (WB) and Immunohistochemistry (IHC) were done to measure eNOS and HIF 1a expression.ResultsHAR in both groups of cirrhotic animals (8W and 12W) were lower compared to controls. Dose response curves to methoxamine revealed lower HAR in both cirrhotic models (8W and 12W) regardless the magnitude of portal resistance. LNMMA corrected the dose response curves in cirrhosis (8W and 12W) to control. WB and IHC show increased protein expression of eNOS and HIF1a in 8W and 12W.ConclusionHepatic arterial resistance is decreased in cirrhosis independent of portal resistance. Vasodilation of the hepatic artery in cirrhosis seems to be influenced by hypoxia rather than increase in portal resistance. Nitric oxide is the main vasodilator.

Ultrasonographic evaluation of abdominal organs after cardiac surgery

BackgroundDisturbances of the hepatosplanchnic region may occur after cardiac operations. Experimental studies have implicated impairment of splanchnic blood supply in major abdominal organ dysfunction after cardiopulmonary bypass (CPB). We investigated the impact of the cardiac operation and CPB on liver, kidney, and renal perfusion and function by means of ultrasonography and biochemical indices in a selected group of cardiac surgery patients. Materials and methodsSeventy five patients scheduled for a major cardiac operation were prospectively included in the study. Criteria for selection were moderate or good left ventricular ejection fraction and absence of previous hepatic or renal impairment. Ultrasound examination of the hepatic and renal vasculature and examination of biochemical parameters were performed on the day preceding the operation (T0), on the first postoperative day (T1), and on the seventh postoperative day (T2). ResultsPortal vein velocity and flow volume increased significantly, whereas hepatic artery velocity and flow volume decreased at T1 in comparison with T0. Hepatic vein indices remained unaffected throughout the observation period. Renal artery velocity and flow decreased, whereas renal pulsatility index and renal resistive index increased at T1 as compared with T0. Aspartate aminotransferase and alanine aminotransferase values were increased as compared with baseline values 24 h postoperatively. All parameters displayed a trend to approach preoperative levels at T2. Strong negative correlations between alanine aminotransferase values at T1 and hepatic artery velocity and flow volume at the same time point were also demonstrated (R = 0.638, P < 0.001 and r = 0.662, P < 0.001, respectively). ConclusionsThe increase in portal vein flow and velocity and the decrease in hepatic artery flow and velocity in the period after CPB might be attributed to the hypothermic bypass technique and the hepatic arterial buffer response, respectively. The decrease in renal blood flow and velocity and the parallel increase in Doppler renal pulsatility index and renal resistive index could be considered as markers of kidney hypoperfusion and intrarenal vasoconstriction. Maintaining a high index of suspicion for the early diagnosis of noncardiac complications in the period after CPB and institution of supportive care in case of compromised splanchnic perfusion are warranted.

Interference of angiotensin II and enalapril with hepatic blood flow regulation.

Acute reduction of portal vein blood flow (Qpv) increases hepatic arterial perfusion (Qha) [the hepatic arterial buffer response (HABR)]. Angiotensin II (AT-II) reduces Qpv, but its effect on HABR is not known. We explored interactions of AT-II and enalapril with hepatic blood flow regulation. Twenty healthy anesthetized pigs were randomized to receive AT-II (n = 8) from 5 to 61 ng/kg per min, enalapril (n = 8) from 3 to 24 μg/kg per h, or saline (n = 4). HABR was assessed by occluding portal vein and expressed as 1) ratio between changes in Qha and Qpv, 2) hepatic arterial conductance (Cha). AT-II infusion increased mean arterial blood pressure from 74 (66-77) mmHg to 116 (109-130) mmHg (median, IQR; P < 0.0001) and decreased cardiac output, Qpv, and renal artery flow (-24%, -28% and -45%, respectively). The fraction of cardiac output of Qha, carotid, and femoral flows increased. With enalapril, blood pressure decreased, whereas cardiac output was maintained with flow redistribution favoring hepatic and renal arteries. In AT-II group, dQha/dQpv increased from 0.06 (0.03, 0.17) to 0.24 (0.13, 0.31) (P = 0.002), but Cha during acute portal vein occlusion decreased from 4.3 (1.6, 6.6) to 2.9 (1.2, 3.7) ml/mmHg (P = 0.003). Both variables remained unchanged in the enalapril group and in controls. AT-II infusion reduces portal flow in parallel with cardiac output and induces a dose-dependent redistribution of flow, favoring brain, hepatic artery, and peripheral tissues at the expense of renal perfusion. During HABR, AT-II decreases Cha but increases Qha compensation, likely as result of increased hepatic arterial perfusion pressure. Enalapril had no effect on HABR.

Analytical Probability Density Calculation for Step Pulse Response of a Single-Ended Buffer With Arbitrary Power-Supply Voltage Fluctuations

An analytical methodology to calculate the probability density functions (PDFs) for the step pulse response of a single-ended buffer with arbitrary power-supply voltage fluctuations is proposed. To validate the theory, a silicon IC with noise-aggressing buffers and a victim buffer was designed, fabricated, and assembled in a printed circuit board (PCB). The overall power distribution network (PDN) of the IC and PCB was modeled from impedance measurements. The PDFs of the step pulse response of the victim buffer with power-supply voltage fluctuations were calculated and validated by comparisons with HSPICE and experimental results. The obtained PDFs due to power-supply voltage fluctuations could be combined with the statistical link simulation methods for quick estimation of bit error rate (BER).

Research progress of hemodynamic signal and liver regeneration

Liver has great ability in regeneration,and liver regeneration is closely related to the prognosis of patients who received liver surgeries.The mechanisms of liver regeneration include biochemical theory and hemodynamic theory.Portal perfusion with moderate pressure is an important factor for starting liver regeneration.Hepatic artery buffer response,fluid shear stress and gasotransmitter play important roles in the liver regeneration.Learning the mechanisms of hemodynamic signal is of great importance for the treatment of liver diseases. Key words: Liver diseases ; Liver regeneration; Hepatectomy; Shear stress; Hepatic arterial buffer response

A Hemodynamic Study to Evaluate the Buffer Response in Cirrhotic Patients Undergoing Liver Transplantation

The physiological regulation of the liver blood flow is a result of a reciprocal portal vein and hepatic artery flow relationship. This mechanism is defined as the hepatic arterial buffer response (HABR). This study was addressed to investigate whether HABR is maintained in denervated grafts in liver transplant recipients. Portal blood flow (PBF) and hepatic arterial resistance index (PI) were measured 6 months after transplantation using Doppler. In each patient we consecutively measured the vasodilator (Ensure Plus PO versus placebo) and vasoconstrictor (isosorbide dinitrate 5 mg SL versus placebo) stimuli. The meal ingestion caused a significant increase of both parameters, PBF (from 1495±260 to 2069±250 mL/min, P&lt;0.05) and PI (from 0.7±0.2 to 0.8±0.2, P&lt;0.05). By contrast, isosorbide dinitrate reduced PBF (from 1660±270 to 1397±250 mL/min, P&lt;0.05) and PI (from 0.7±0.2 to 0.5±0.2, P&lt;0.05). We show that PBF and PI are reciprocally modified with the administration of vasoconstrictor and vasodilator stimuli. These results suggest the persistence of the HABR in a denervated human model, suggesting that this mechanism is independent of the regulation from the autonomic nervous system.

Pseudoparallel Channel Sign on Ultrasonography in Alcoholic Hepatitis

Pseudoparallel Channel Sign on Ultrasonography in Alcoholic Hepatitis

Nuclear medicine dynamic investigations in the diagnosis of Budd-Chiari syndrome.

To investigate the hepatic hemodynamics in the Budd-Chiari syndrome (BCS) using per-rectal portal scintigraphy (PRPS) and liver angioscintigraphy (LAS). Fourteen consecutive patients with BCS were evaluated by PRPS between 2003 and 2012. Ten of them underwent LAS and liver scan (LS) with Tc-99m colloid. Eleven patients had clinical manifestations and three were asymptomatic, incidentally diagnosed at PRPS. The control group included 15 healthy subjects. We used new parameters at PRPS, the liver transit time of portal inflow and the blood circulation time between the right heart and liver. PRPS offered information on the hepatic areas missing venous outflow or portal inflow, length and extent of the lesions, open portosystemic shunts (PSS), involvement of the caudate lobe (CL) as an intrahepatic shunt and flow reversal in the splenic vein. LAS was useful in the differential diagnosis between the BCS and portal obstructions, highlighting the hepatic artery buffer response and reversed portal flow. LS offered complementary data, especially on the CL. We described three hemodynamic categories of the BCS with several subtypes and stages, based on the finding that perfusion changes depend on the initial number and succession in time of the hepatic veins (HVs) obstructions. Obstruction of one hepatic vein (HV) did not cause opening of PSS. The BCS debuted by common obstruction of two HVs had different hemodynamic aspects in acute and chronic stages after subsequent obstruction of the third HV. In chronic stages, obstruction of two HVs resulted in opening of PSS. The BCS, determined by thrombosis of the terminal part of the inferior vena cava, presented in the acute stage with open PSS with low speed flow. At least several weeks are required in the obstructions of two or three HVs for the spontaneous opening of dynamically efficient PSS. The CL seems to have only a transient important role of intrahepatic shunt in several types of the BCS. Dynamic nuclear medicine investigations assess the extent and length of hepatic venous obstructions, open collaterals, areas without portal inflow, hemodynamic function of the CL and reverse venous flow.

Hemodynamic changes in the hepatic circulation after the modulation of the splenic circulation in an in vivo human experimental model

Recent advances in liver surgery have highlighted the effects of the splenic circulation on the hepatic circulation with respect to the hepatic arterial buffer response (HABR). The aim of the present study was to investigate the actual hemodynamic effects of splenic artery embolization/ligation and splenectomy on the hepatic circulation in patients who underwent pancreaticoduodenectomy through in vivo experimental models. In vivo models of splenic artery embolization/ligation (only splenic artery clamping) and splenectomy (simultaneous clamping of both the splenic artery and the splenic vein) were created in 40 patients who underwent pancreaticoduodenectomy for various reasons. The portal venous flow velocity, the portal venous flow volume, the hepatic arterial flow velocity, and the hepatic arterial resistance index were measured with color Doppler ultrasonography. Clamping of the splenic artery induced an immediate and significant increase (16%) in the hepatic artery velocity (P < 0.001), and the portal venous flow also decreased significantly (10%, P = 0.03). Fifteen minutes after the clamping of the splenic artery, the hepatic artery velocity remained significantly increased at the level of the initial clamping, and the portal venous flow significantly decreased (16%, P < 0.001). Clamping of the splenic vein, which was performed after the clamping of the splenic artery, resulted in an immediate and significant decrease (30%) in the portal venous flow (P < 0.001), but the hepatic arterial flow was not affected. Fifteen minutes after the clamping of the splenic vein, there was no change in the portal flow, which remained significantly lower (28%) than the flow in controls, whereas the hepatic arterial flow further significantly increased (31%, P < 0.001). In conclusion, our findings indicate that both splenic artery embolization/ligation and splenectomy are effective for increasing hepatic arterial flow and decreasing portal flow, with splenectomy providing a greater advantage. The HABR underlies these hemodynamic changes.

Regarding “liver stiffness is influenced by a standardized meal in patients with chronic hepatitis C virus at different stages of fibrotic evolution”

We congratulate Arena et al.1 for their interesting article regarding the confounding effect of a meal on the accuracy of liver stiffness (LS) measurements for the prediction of fibrosis stage in patients with chronic hepatitis C virus (HCV) hepatitis. In that study the most prominent postprandial increase in LS was observed in patients with cirrhosis. Hemodynamic parameters were not measured, but it is suggested that the postprandial changes in LS are likely consequent to the adaptation of the hepatic microcirculation to increased portal blood flow (PBF) and to the postprandial increase in portal pressure. We recently published a study2 involving 19 patients with cirrhosis and portal hypertension in whom LS and hepatic hemodynamics were measured by Doppler-ultrasonography at baseline and 30 minutes after the ingestion of a standardized meal similar to that used by Arena et al. In a subgroup of 10 patients, the baseline and postprandial hepatic venous pressure gradient (HVPG) were also measured. In agreement to what was described by Arena et al.,1 showing that most patients irrespective of the stage of fibrosis had a peak increase of LS 30 minutes after the meal, in our series postprandial hyperemia (confirmed by a marked increase in PBF, +33 ± 31%, P < 0.0001 versus baseline) was accompanied by a marked increase in LS (+27 ± 33%; P < 0.0001). However, we observed that postprandial changes in LS did not correlate with the changes in PBF. Similarly, in patients in whom HVPG was measured, LS changes did not mirror the HVPG increase after the standardized meal. In contrast, postprandial changes in LS were directly correlated with changes in hepatic artery blood flow (r = 0.658; P = 0.002), so that in patients showing the expected postprandial decrease in hepatic artery blood flow (reflecting the “buffer response” to increased PBF after a meal) the LS increase was significantly attenuated as compared with patients lacking this adaptive mechanism (+12 ± 21% versus +62 ± 29%, P < 0.0001). Altogether, our results suggest that the postprandial increase in LS in cirrhosis cannot be explained by the increase in PBF and portal pressure, while it seems at least in part dependent on changes in the arterial component of hepatic blood flow. Since extensive formation of collaterals in advanced portal hypertension leads to increased dependence of the hepatic blood flow on its arterial component, and since hepatic artery buffer response is reduced in cirrhosis,3 a greater postprandial increase in LS should be anticipated in overt cirrhosis. Annalisa Berzigotti, M.D. Juan G. Abraldes, M.D. Jaume Bosch, M.D. Hepatic Hemodynamic Laboratory, Liver Unit, IDIBAPS and CIBERehd, Hospital Clinic, Barcelona, Spain

Smooth muscle contractile diversity in the control of regional circulations

Each regional circulation has unique requirements for blood flow and thus unique mechanisms by which it is regulated. In this review we consider the role of smooth muscle contractile diversity in determining the unique properties of selected regional circulations and its potential influence on drug targeting in disease. Functionally smooth muscle diversity can be dichotomized into fast versus slow contractile gene programs, giving rise to phasic versus tonic smooth muscle phenotypes, respectively. Large conduit vessel smooth muscle is of the tonic phenotype; in contrast, there is great smooth muscle contractile diversity in the other parts of the vascular system. In the renal circulation, afferent and efferent arterioles are arranged in series and determine glomerular filtration rate. The afferent arteriole has features of phasic smooth muscle, whereas the efferent arteriole has features of tonic smooth muscle. In the splanchnic circulation, the portal vein and hepatic artery are arranged in parallel and supply blood for detoxification and metabolism to the liver. Unique features of this circulation include the hepatic-arterial buffer response to regulate blood flow and the phasic contractile properties of the portal vein. Unique features of the pulmonary circulation include the low vascular resistance and hypoxic pulmonary vasoconstriction, the latter attribute inherent to the smooth muscle cells but the mechanism uncertain. We consider how these unique properties may allow for selective drug targeting of regional circulations for therapeutic benefit and point out gaps in our knowledge and areas in need of further investigation.

Reproductive system of a mixed-mating plant responds to climate perturbation by increased selfing

How plants respond to climatic perturbations, which are forecasted to increase in frequency and intensity, is difficult to predict because of the buffering effects of plasticity. Compensatory adjustments may maintain fecundity and recruitment, or delay negative changes that are inevitable but not immediately evident. We imposed a climate perturbation of warming and drought on a mixed-mating perennial violet, testing for adjustments in growth, reproduction and mortality. We observed several plasticity-based buffering responses, such that the climatic perturbation did not alter population structure. The most substantial reproductive adjustments, however, involved selfing, with a 45% increase in self-pollination by chasmogamous flowers, a 61% increase in the number of cleistogamous flowers that produced at least one fruit and an overall 15% increase in fruit production from selfed cleistogamous flowers. Reproductive assurance thus compensated for environmental change, including low pollinator visitation that occurred independently of our climate treatment. There was also no immediate evidence for inbreeding depression. Our work indicates that plants with vegetative and reproductive flexibility may not be immediately and negatively affected by a climatic perturbation. The stabilizing effects of these reproductive responses in the long term, however, may depend on the implications of significantly elevated levels of selfing.

THU0581 Spousal Protective Buffering is Related to a Lower Physical and Mental Quality of Life in Patients with Sjögren’s Syndrome

BackgroundPatients with Sjögren’s syndrome are hampered by dryness and fatigue, which impact on quality of life.1,2 Social support –such as the help and understanding of spouses– is assumed to have...

Effect of Meal Ingestion on Liver Stiffness in Patients with Cirrhosis and Portal Hypertension

Background and AimsLiver stiffness is increasingly used in the non-invasive evaluation of chronic liver diseases. Liver stiffness correlates with hepatic venous pressure gradient (HVPG) in patients with cirrhosis and holds prognostic value in this population. Hence, accuracy in its measurement is needed. Several factors independent of fibrosis influence liver stiffness, but there is insufficient information on whether meal ingestion modifies liver stiffness in cirrhosis. We investigated the changes in liver stiffness occurring after the ingestion of a liquid standard test meal in this population.MethodsIn 19 patients with cirrhosis and esophageal varices (9 alcoholic, 9 HCV-related, 1 NASH; Child score 6.9±1.8), liver stiffness (transient elastography), portal blood flow (PBF) and hepatic artery blood flow (HABF) (Doppler-Ultrasound) were measured before and 30 minutes after receiving a standard mixed liquid meal. In 10 the HVPG changes were also measured.ResultsPost-prandial hyperemia was accompanied by a marked increase in liver stiffness (+27±33%; p<0.0001). Changes in liver stiffness did not correlate with PBF changes, but directly correlated with HABF changes (r = 0.658; p = 0.002). After the meal, those patients showing a decrease in HABF (n = 13) had a less marked increase of liver stiffness as compared to patients in whom HABF increased (n = 6; +12±21% vs. +62±29%,p<0.0001). As expected, post-prandial hyperemia was associated with an increase in HVPG (n = 10; +26±13%, p = 0.003), but changes in liver stiffness did not correlate with HVPG changes.ConclusionsLiver stiffness increases markedly after a liquid test meal in patients with cirrhosis, suggesting that its measurement should be performed in standardized fasting conditions. The hepatic artery buffer response appears an important factor modulating postprandial changes of liver stiffness. The post-prandial increase in HVPG cannot be predicted by changes in liver stiffness.

Occurrence of the Connecticut Warbler Increases with Size of Patches of Coniferous Forest

Abstract. The Connecticut Warbler (Oporornis agilis) is a rare and declining neotropical migrant that breeds in the north-central United States and south-central Canada. To better understand the species' habitat needs, we analyzed 371 observations of the Connecticut Warbler over 18 years at 86 sites in 28 stands of forest in northern Minnesota. We considered the habitat and landscape at three spatial scales (buffer radii of 100, 500, and 1000 m) and regressed combinations of habitat variables with two response variables, the Connecticut Warbler's abundance (the total number of individuals ever recorded at a site or stand, with a zero-inflated negative binomial distribution) and frequency (the number of years recorded out of 18, with logistic regression). From a subset of models retained on the basis of Akaike's information criterion, we calculated model-averaged predictions for each combination of buffer size and response variable. Models based on Connecticut Warbler frequency at the 1000-m buffer perform...

Habitat loss and fragmentation affecting mammal and bird communities—The role of interspecific competition and individual space use

Fragmentation and loss of habitat are major threats to animal communities and are therefore important to conservation. Due to the complexity of the interplay of spatial effects and community processes, our mechanistic understanding of how communities respond to such landscape changes is still poor. Modelling studies have mostly focused on elucidating the principles of community response to fragmentation and habitat loss at relatively large spatial and temporal scales relevant to metacommunity dynamics. Yet, it has been shown that also small scale processes, like foraging behaviour, space use by individuals and local resource competition are also important factors. However, most studies that consider these smaller scales are designed for single species and are characterized by high model complexity. Hence, they are not easily applicable to ecological communities of interacting individuals. To fill this gap, we apply an allometric model of individual home range formation to investigate the effects of habitat loss and fragmentation on mammal and bird communities, and, in this context, to investigate the role of interspecific competition and individual space use. Results show a similar response of both taxa to habitat loss. Community composition is shifted towards higher frequency of relatively small animals. The exponent and the 95%-quantile of the individual size distribution (ISD, described as a power law distribution) of the emerging communities show threshold behaviour with decreasing habitat area. Fragmentation per se has a similar and strong effect on mammals, but not on birds. The ISDs of bird communities were insensitive to fragmentation at the small scales considered here. These patterns can be explained by competitive release taking place in interacting animal communities, with the exception of bird's buffering response to fragmentation, presumably by adjusting the size of their home ranges. These results reflect consequences of higher mobility of birds compared to mammals of the same size and the importance of considering competitive interaction, particularly for mammal communities, in response to landscape fragmentation. Our allometric approach enables scaling up from individual physiology and foraging behaviour to terrestrial communities, and disentangling the role of individual space use and interspecific competition in controlling the response of mammal and bird communities to landscape changes.

Xenon: A Solution for Anesthesia in Liver Disease?

Xenon: A Solution for Anesthesia in Liver Disease?

Modeling the hepatic arterial buffer response in the liver

In this paper we present an electrical analog model for the hepatic arterial buffer response (HABR), an intrinsic regulation mechanism in the liver whereby the arterial flow counteracts the changes in portal venous flow. The model itself is a substantial simplification of a previously published model, with nonlinear arterial and portal resistors introduced to account for the dynamic HABR effects. We calibrate the baseline model using published hemodynamic data, and then perform a virtual portal occlusion simulation where the portal vein is half or fully occluded. The simulation results, which suggest that the increased arterial flow cannot fully compensate lost portal perfusion, are consistent with clinical reports and animal model findings. Since HABR functions in both the whole liver and liver graft after transplantation, we also simulate blood flow in a virtual right-lobe graft by adjusting the electronic component parameters in the electric circuit, and our model is able to reproduce the portal venous hyperperfusion and hepatic arterial hypoperfusion conditions due to the HABR effects.