Effects of posture change on the hemodynamics of the liver

BACKGROUND/AIMS: According to our experience, blood flow in the portal vein may alter according to body posture. It is reported that decreased portal venous flow immediately gives rise to significantly increased blood flow in the hepatic artery. To gain further insight into blood flow changes affected by posture, we examined blood flows in the portal vein, hepatic artery and hepatic vein at different postures. METHODOLOGY: Using a Doppler ultrasound system, the hemodynamics of the portal vein, right hepatic artery, and hepatic vein were examined in 35 patients at supine and left decubitus positions. RESULTS: Portal vein blood flow volumes were significantly lower in the left decubitus position than in the supine. In the right hepatic artery, the left decubitus position gave significantly higher blood flow velocity values than the supine. CONCLUSIONS: Our results indicated that upon change of posture from the supine to left decubitus position, portal vein flow velocity was reduced and hepatic artery flow velocity increased. Changes in portal and hepatic arterial flows by changing posture may be explained by decreased portal flow as a direct result of changed posture, leading to increased hepatic arterial flow to maintain total hepatic blood inflow.     

Hemodynamics during liver transplantation: the interactions between cardiac output and portal venous and hepatic arterial flows.

Liver blood flow and systemic hemodynamics were measured intraoperatively in 34 patients after liver transplantation. Ultrasound transit-time flow probes measured hepatic arterial and portal venous flow over 10 to 75 min 1 to 3 hr after reperfusion. Cardiac output was measured by thermodilution. Mean cardiac output was 9.5 +/- 2.8 L/min; the mean total liver blood flow of 2,091 +/- 932 ml/min was 23% +/- 11% of cardiac output. Mean portal flow of 1,808 +/- 929 ml/min was disproportionately high at 85% +/- 10% of total liver blood flow. Correlation analysis showed a significant (p less than 0.01; r = 0.42) correlation between cardiac output and portal venous flow and a trend toward negative correlation (p = 0.087) between cardiac output and hepatic arterial flow. These data show that increased flow in the newly transplanted liver is predominantly portal venous flow and is associated with high cardiac output and reduced hepatic arterial flow. In the last 13 patients studied, portal flow was reduced by 50% and the hepatic artery response was measured. We saw a significant (p less than 0.05) increase in hepatic artery flow from 322 +/- 228 to 419 +/- 271 ml/min, indicating an intact hepatic arterial buffer response. The hepatic artery response also showed that it is a reversible rather than a fixed resistance that contributes to the low hepatic artery flow in these patients.     

Hepatic arterial and portal flow in cardiogenic and hemorrhagic shock in awake dogs

The changes in liver blood flow produced by experimental cardiogenic and hemorrhagic shock are relatively unexplored. Fifteen unanesthetized dogs in which electromagnetic blood flow transducers had been implanted on the common hepatic artery and portal vein were subjected to acute myocardial infarction by mercury embolization of the circumflex coronary artery. Another group of ten dogs were bled to an arterial pressure of 40 mmHg and maintained at that level for 2 hours before reinfusion. Six additional dogs in which blood flow transducers had been implanted on the superior mesenteric artery and portal vein also were subjected to hemorrhage. In three of the six, phenoxybenzamine was infused directly into the superior mesenteric artery 45 minutes prior to bleed-out. During cardiogenic shock, both hepatic arterial and protal venous flow fell. However, whereas protal flow continued to fall, eventually stabilizing at values 36 +/- 3% of control, hepatic arterial flow subsequently rose, reaching values 93 +/- 9% above control. Total liver blood flow, after an initial decline to 53 +/- 4% of control levels rose as a result of the increased hepatic arterial flow to 73 +/- 4% of control values. During hemorrhage, both hepatic arterial and protal venous flows decreased as aortic pressure fell. Within 5 minutes of reinfusion, hepatic arterial flow surpassed its control values. Portal flow also increased but, on a percentage basis, not to so great an extent. Flow in hepatic artery remained high for 40 minutes after reinfusion, whereas portal flow rapidly decreased to levels seen at the end of hemorrhage. In hemorrhage without alpha-adrenergic receptor blockade the superior mesenteric bed constricted, thereby supporting systemic pressure. With alpha-adrenergic blockade, however, mesenteric flow became pressure-dependent and no longer acted as a homeostatic mechanism.     

Direct measurement of hepatic blood flow in native and transplanted organs, with accompanying systemic hemodynamics.

The purpose of this study was to investigate intraoperatively a population of patients with end-stage liver disease before and after liver transplantation with respect to (a) the range of hepatic and systemic hemodynamics and their changes associated with transplantation and (b) the ability to identify native hemodynamic correlates with specific diagnostic groups. Hepatic artery and portal vein blood flows were determined with square-wave electromagnetic flowmetry. Significant differences related to the type of preservation solution used--Euro-Collins or University of Wisconsin--were identified in some hepatic and systemic hemodynamic measurements from the graft livers. Specifically, cardiac output, total liver blood flow and liver weight were significantly increased in the Euro-Collins group compared with the native and University of Wisconsin groups. Hepatic artery flow was significantly greater and portal vein pressure was significantly lower in the University of Wisconsin group than in the native or Euro-Collins group. In general, comparing the graft and native livers, hepatic artery and portal vein blood flow increased significantly after transplantation, as did hepatic oxygen consumption. Portal vein pressures were dramatically reduced, but systemic arterial pressure remained remarkably constant. The percentage of cardiac output going to the liver increased, as did the portal vein percentage of the total liver blood flow. Diagnostic groups could not clearly be associated with characteristic native liver or systemic hemodynamics. Hemodynamics may be associated more with the stage of the disease process than the disease itself.     

Hepatic vasculature: a conceptual review.

The hepatic circulation is reviewed with emphasis on the role of hepatic blood vessels in hepatic and homeostatic functions. Contrasts are made with resistance, capacitance, and fluid exchange functions in other better known vascular beds. Hemodynamic changes that produce shifts in fluid exchange in other tissues are without effect in the liver. Elevations of hepatic venous pressure are transferred quantitatively to the sinusoids and result in prolonged, massive fluid filtration into the abdominal cavity. Other factors that are involved with control of fluid exchange are discussed. The liver contains a large volume of blood which can be rapidly mobilized during hemorrhage. The hepatic circulation is highly sensitive to changes in circulating blood volume and serves as a major buffer for expanded or contracted blood volume. Control of hepatic blood flow and the reciprocal relationship between portal and hepatic arterial flow is discussed. Changes in hepatic blood flow produce marked changes in hepatic clearance rates of a wide variety of compounds. It is concluded that the hepatic artery is not controlled by local tissue metabolism but rather is controlled by an, as yet unknown, mechanism that tends to maintain hepatic blood flow (and therefore clearance rates) constant.     

Hepatic presinusoidal sphincters affected by altered arterial pressure and flow, venous pressure, and nerve stimulation

Alterations in hepatic circulation and oxygen uptake were monitored using an intact feline liver preparation with arterial and portal blood flows measured separately and hepatic venous pressure under experimental control. Oxygen extraction ratios, if interpreted cautiously, can be used to indicate sphincter-like control of diffusion parameters in the tissues. Presinusoidal (precapillary) sphincters do not alter fluid exchange parameters in the liver. The results shown here are interpreted as providing evidence that sphincters or sphincter-like segments of the hepatic vasculature do, however, affect diffusion parameters. Constriction of sphincters is associated with a reduced oxygen extraction ratio, dilation with increased extraction. The sphincters are initially constricted by hepatic nerve stimulation but show a secondary dilation due to maintained reduction in conductance of the hepatic artery (upstream). Sphincter dilation, indicated by increased oxygen extraction under selective experimental conditions, was suggested. Elevations in arterial blood pressure produced myogenic arterial constriction which resulted in secondary sphincter dilation. Similarly, graded occlusion of the hepatic artery resulted in sphincter dilation. Sphincters appear to be controlled by blood flow changes since oxygen extraction changes were correlated with changes in blood flow but not with changes in hepatic oxygen delivery. Myogenic stimuli do not appear to affect sphincters since elevated hepatic venous pressure did not cause sphincter constriction, nor did in impair oxygen uptake.     

Change in portal flow after liver transplantation: effect on hepatic arterial resistance indices and role of spleen size

Information on changes in splanchnic hemodynamics after liver transplantation is incomplete. In particular, data on long-term changes are lacking, and the relationship between changes in arterial and portal parameters is still under debate. The effect of liver transplantation on splanchnic hemodynamics was analyzed with echo-Doppler in 41 patients with cirrhosis who were followed for up to 4 years. Doppler parameters were also evaluated in 7 patients transplanted for acute liver failure and in 35 controls. In cirrhotics, portal blood velocity and flow increased immediately after transplantation (from 9.1 plus minus 3.7 cm/sec to 38.3 plus minus 14.6 and from 808 plus minus 479 mL/min to 2,817 plus minus 1,153, respectively, P <.001). Hepatic arterial resistance index (pulsatility index) also augmented (from 1.36 plus minus 0.32 to 2.34 plus minus 1.29, P <.001) and was correlated with portal blood velocity and flow. The early changes in these parameters were related, in agreement with the hepatic buffer response theory. Portal flow returned to normal values after 2 years. Superior mesenteric artery flow normalized after 3 to 6 months. Splenomegaly persisted after 4 years, when spleen size was related to portal blood flow. In 7 patients transplanted for acute liver failure, portal flow, and hepatic arterial resistance index were normal after transplantation. In conclusion, a high portal flow was present in cirrhotics until 2 years after transplantation, probably because of maintenance of elevated splenic flow. An early increase in hepatic arterial resistance indices is a common finding, but it is transient and is related to the increase in portal blood flow. A normal time course of portal-hepatic hemodynamics was detected in patients transplanted for acute liver failure.     

Hepatic hemodynamic changes during liver transplantation: A review

Liver transplantation is performed in the recent decades with great improvements not only technically but also conceptually. However, there is still lack of consensus about the optimal hemodynamic characteristics during liver transplantation. The representative hemodynamic parameters include portal vein pressure, portal vein flow, and hepatic venous pressure gradient; however, there are still others potential valuable parameters, such as total liver inflow and hepatic artery flow. All the parameters are correlated closely and some internal modulating mechanisms, like hepatic arterial buffer response, occur to maintain stable hepatic inflow. To distinguish the unique importance of each hepatic and systemic parameter in different states during liver transplantation, we reviewed the published data and also conducted two transplant cases with different surgical strategies applied to achieve ideal portal inflow and pressure.     

Hepatic circulation in acute hemorrhage with reference to renal circulation.

Studies were made on the hemodynamics in the liver and kidney during hemorrhage and retransfusion, using 20 dogs with or without hepatic periarterial nerve plexus, anaesthetized with sodium pentobarbital. The results were as follows. In 14 dogs in which the hepatic periarterial nerve plexus was left intact (Group A), the averages of the hepatic arterial flow (HAF), portal venous pressure (PVP), portal venous flow (PVF), and flow in the right renal artery (RAF) decreased significantly to 38, 64, 35, and 25%, respectively of the control levels when the abdominal aortic pressure (ABP) fell to 40 mm Hg (36% of the control level) during hemorrhage. At the same time the portal venous resistance (PVR) and the right renal vascular resistance (RVR) increased greatly and the hepatic arterial resistance (HAR) either increased or decreased in different dogs. During retransfusion the ABP and vascular resistance returned to nearly the control levels, the PVF increased beyond the control level. In 6 dogs in which the nerve plexus was resected (Group B), the decreases in the HAF and RAF during hemorrhage were not significantly different from those in Group A. These results may suggest the following. The decrease in the HAF during hemorrhage seems to be mostly a passive change resulting from decrease in the systemic blood pressure. Neurogenic regulation may be a little. Further, the existence of the humoral regulation and autoregulation in the HAF were suggested in some cases. While, the responsibilities to hemorrhage and retransfusion appear to be different among the examined three vessels, i.e. the hepatic artery, portal vein, and renal artery. No definite interrelation was seen between the hepatic and renal circulations.     

Effects of ethanol and wine on hepatic arterial and portal venous flows in conscious dogs.

The effects of ethanol and wine on hepatic arterial and portal venous flows were examined in conscious dogs. Ethanol was given intravenously or intragastrically, and red wine (ethanol: 14%) was given intragastrically over 30 min. Intravenous ethanol (0.8 g/kg) and intragastric ethanol (14% vol/vol) increased hepatic arterial flow, which remained elevated for 60 min after the cessation of ethanol administration. Ethanol also increased portal venous flow. Portal venous flow returned gradually toward basal levels after the cessation of intravenous ethanol infusion, whereas it remained elevated even after the cessation of intragastric ethanol. Intragastric wine increased hepatic arterial and portal venous flows. In contrast to intragastric ethanol, hepatic arterial flow continued to rise after the cessation of intragastric wine infusion, while portal venous flow returned toward basal levels. We conclude that, though both ethanol and wine increase hepatic blood flow, the responses of hepatic arterial and portal venous flows differ substantially among intravenous ethanol, intragastric ethanol and intragastric wine.     

Regulation of hepatic blood flow: the hepatic arterial buffer response revisited

The interest in the liver dates back to ancient times when it was considered to be the seat of life processes. The liver is indeed essential to life,not only due to its complex functions in biosynthesis,metabolism and clearance,but also its dramatic role as the blood volume reservoir. Among parenchymal organs,blood flow to the liver is unique due to the dual supply from the portal vein and the hepatic artery. Knowledge of the mutual communication of both the hepatic artery and the portal vein is essential to understand hepatic physiology and pathophysiology. To distinguish the individual importance of each of these inflows in normal and abnormal states is still a challenging task and the subject of on-going research. A central mechanism that controls and allows constancy of hepatic blood flow is the hepatic arterial buffer response. The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease. We exclusively focus on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation,as well as inflammatory and chronic liver diseases. We do not consider the hepatic microvascular anatomy,as this has been the subject of another recent review.     

The Influence of Flow and Hematocrit on the Laser Doppler Flux Signal from the Surface of the Perfused Pig Liver

Objective: We tested the hypothesis that the measurement volume of the laser Doppler flowmeter (LDF) is too small to provide reliable quantitative estimates of total liver blood flow of large mammals, such as the pig. Methods: In a perfused pig liver, the influence of changing (i) hepatic arterial (HA) and portal venous flows individually (n = 9), (ii) HA flow at fixed portal venous flow (50%, 70%, and 100% expected total liver blood flow), and (iii) hematocrit (0–30%) at fixed total liver blood flow on LDF flux was tested (n = 8). Results: Linearity of LDF with hepatic arterial flow and portal venous flow was confirmed; however, the slope of the regression lines was higher for hepatic artery [1.92 ± 0.60 (SD)] than portal vein perfused livers (0.66 ± 0.34; P < 0.001). With portal venous flow at 50% and 70% total liver blood flow, changing hepatic arterial flow produced linear LDF versus flow responses, but at 100% total liver blood flow, linearity was achieved in only 6/9 livers. The coefficient of variation for the slopes of regression lines was always > 30%. At constant total liver blood flow (100 ml/min per 100 g), LDF response decreased linearly by a factor of about 2 on changing the hematocrit from 30% to 5% and markedly fell as the hematocrit was further decreased to zero. Conclusions: These results suggest that (i) the LDF flux signal from the liver surface provides a poor measure of hepatic microcirculatory blood flow during changes in total liver blood flow as the LDF responds with about three times greater sensitivity to changes in hepatic arterial than in portal venous flow, and (ii) when hematocrit is falling, LDF may underestimate hepatic perfusion to a significant extent. In addition, due to high measurement variability, the LDF flux signal cannot be quantified in absolute perfusion units.     

Influence of dopamine on liver dynamics in hemorrhagic shock

The present study was conducted to examine the effect of dopamine on arterial blood pressure, liver blood flow, cathepsin D activity, and free amino nitrogen concentration in hemorrhagic shock. Dopamine at a dose of 4 microgram/kg/min increased both mean arterial blood pressure and liver blood flow in postoligemic shock, but failed to prevent the marked increases in circulating cathepsin D and free amino nitrogen. In fact, dopamine infusion resulted in an increased plasma cathepsin D activity in shock. This increased accumulation of a lysosomal marker enzyme probably results from increased washout of the enzyme from the splanchnic or hepatic vascular bed in response to increased blood flow in these areas rather than from a direct effect of dopamine on lysosomal integrity. The increase in hepatic artery and portal vein flows appeared to result from stimulation of dopaminergic receptors since the dopamine dose was in the dopaminergic range and because haloperidol, a dopamine blocker, abolished the improved hemodynamic effects of dopamine. This study suggests that dopamine benefits the animal in hemorrhagic shock hemodynamically, but does not reverse the metabolic and cellular problems in shock. Perhaps, in combination with a drug opposing the biochemical basis of shock, dopamine may provide a greater anti-shock action.     

Effect of ethanol on splanchnic hemodynamics in awake and unrestrained rats with portal hypertension

Alcoholic liver disease is frequently accompanied by portal hypertension. We have previously shown that alcohol intake in awake, unrestrained rats is followed by an increase in portal tributary blood flow. In this study, the effect of ethanol on splanchnic hemodynamics in rats with portal hypertension was analyzed. Portal hypertension was induced by partial ligation of the portal vein. This procedure resulted in an increase in portal tributary and hepatic arterial blood flows compared to sham-operated animals. Ethanol (2 gm per kg, oral) increased portal tributary blood flow in both sham-operated and portal vein-ligated rats (sham + water = 37.6 +/- 1.4; sham + ethanol = 63.1 +/- 1.9; p less than 0.01; partial portal vein stenosis + water = 53.2 +/- 3.3; partial portal vein stenosis + ethanol = 69.5 +/- 2.2 ml.kg-1.min-1; p less than 0.01). In sham-operated rats, hepatic artery blood flow was unchanged following ethanol (sham + water = 6.6 +/- 0.7; sham + ethanol = 7.1 +/- 1.0 ml.kg-1.min-1), whereas in portal vein-ligated rats, flow was increased (partial portal vein stenosis + water = 13.7 +/- 1.4; partial portal vein stenosis + ethanol = 19.8 +/- 1.1 ml.kg-1.min-1; p less than 0.025). The adenosine receptor blocker 8-phenyltheophylline suppressed only the ethanol-induced increase in both portal tributary and hepatic artery blood flows in portal vein-ligated rats. The increases in hepatic artery and portal tributary blood flows observed in portal vein-ligated rats without ethanol were not influenced by 8-phenyltheophylline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic arterial blood flow in large hepatocellular carcinoma with or without portal vein thrombosis: assessment by transcutaneous duplex Doppler sonography

BACKGROUND: As liver cirrhosis progresses, the portal venous blood (PVBF) flow decreases, accompanied by an increase in hepatic arterial blood flow. Large hepatocellular carcinoma is a hypervascular tumour with a rapid growth, which seems to require an increase of the tumoral arterial blood flow. Furthermore, hepatocellular carcinoma is frequently associated with portal vein thrombosis, which subsequently impedes portal blood supply. METHODS: The purpose of our study was to estimate alterations in the hepatic arterial blood flow in large hepatocellular carcinomas occurring in liver cirrhosis, in comparison with liver cirrhosis and controls. Liver blood flow measurements were determined by duplex Doppler sonography in 47 patients with large hepatocellular carcinomas (13 with portal vein thrombosis and 34 without this thrombosis), 42 liver cirrhosis patients and 30 controls. The Doppler perfusion index was calculated as the ratio of hepatic arterial blood flow to total hepatic blood flow. RESULTS: The patients with liver cirrhosis had a significant increase of hepatic arterial blood flow as compared to controls (P < 0.001), accompanied by a significant reduction in PVBF (P < 0.005). As a result, the Doppler perfusion index was increased in patients with liver cirrhosis as compared to controls (P < 0.001). The hepatic arterial blood flow was increased in patients with hepatocellular carcinoma but without portal vein thrombosis as compared to the cirrhotic patients (P < 0.001), with a significant reduction of PVBF (P < 0.001). Hepatic arterial blood flow was also increased in patients with both hepatocellular carcinoma and portal vein thrombosis as compared to the patients without this thrombosis (P < 0.001). CONCLUSION: These results suggest that in large hepatocellular carcinomas there is a decreased PVBF, accompanied by an increased hepatic arterial blood flow. The hepatic arterial buffer response seems to be active in hepatocellular carcinomas and maintains liver perfusion to adequate levels.     

Liver angioscintigraphy: clinical applications

Liver angioscintigraphy (LAS) is a radio-isotope method for the investigation of liver perfusion and its alteration in various hepatic diseases. It measures the arterial and portal venous fractions of total liver blood flow. The percentage of liver blood flow supplied by hepatic artery is estimated mathematically by the hepatic perfusion index (HPI), normally between 25 % and 40 %. The decrease of portal blood flow in liver cirrhosis is compensated ("buffer" mechanisms) by increased arterial supply, with higher HPI value. For a patient with chronic liver disease, HPI over 50% suggests arterialization of hepatic perfusion, guiding the diagnose to liver cirrhosis. Splenic curve is completing the diagnostic information of the hepatic curve. Corroborated with per rectal scintigraphy and liver SPECT, LAS offers a good hemodynamic staging of chronic inflammatory liver diseases. Malignant tumors (primitive or metastases) increase the arterial supply of the liver and decrease the portal flow, HPI being over 50% (currently 65 % - 90 %). Benign tumors do not change portal/arterial liver blood flow ratio. SPECT or non-scintigraphic morphological investigations increase the diagnostic value of LAS for primitive liver tumors. Liver cancer occurring on cirrhosis is a limitative factor for LAS. Hepatic metastases increase the arterial perfusion (and HPI value) very quickly, before their size allows morphologic imaging diagnosis. LAS is therefore an early method to diagnose liver metastases being especially used in colorectal cancer. Other clinical applications of LAS are: follow up of liver toxicity of drugs, evaluation of portal vein permeability, post surgery follow up of the liver tumor patients.     

Hepatic arterial buffer response in patients with advanced cirrhosis

Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion. Accordingly, patients with severe cirrhosis should have impaired HABR after TIPS implantation. Therefore, the aim of this study was to investigate the effect of TIPS on HABR as reflected by changes in resistance index (RI) of the hepatic artery. A total of 366 patients with cirrhosis (Child-Pugh class A, 106; class B, 168; class C, 92) underwent duplex Doppler ultrasonographic examination with determination of RI and maximal flow velocity in the portal vein before and 1 month after TIPS placement. Portosystemic pressure gradient was determined before and after TIPS placement. In 29 patients with hepatofugal portal blood flow, RI was significantly lower than in 337 patients with hepatopetal flow (0.63 plus minus 0.02 vs. 0.69 plus minus 0.01; P <.001). TIPS induced a significant decrease of the RI in patients with hepatopetal flow (RI, 0.69 plus minus 0.01 before vs. 0.64 plus minus 0.01 after TIPS; P =.001) but not in patients with hepatofugal flow (RI, 0.63 plus minus 0.02 before vs. 0.63 plus minus 0.02 after TIPS; NS). This response was not dependent on the Child-Pugh class. In conclusion, our results suggest that some degree of HABR is preserved even in patients with advanced cirrhosis with significant portal hypertension.     

Regulatory processes interacting to maintain hepatic blood flow constancy: Vascular compliance, hepatic arterial buffer response, hepatorenal reflex, liver regeneration, escape from vasoconstriction

Constancy of hepatic blood flow (HBF) is crucial for several homeostatic roles. The present conceptual review focuses on interrelated mechanisms that act to maintain a constant HBF per liver mass. The liver cannot directly control portal blood flow (PF); therefore, these mechanisms largely operate to compensate for PF changes. A reduction in PF leads to reduced intrahepatic distending pressure, resulting in the highly compliant hepatic vasculature passively expelling up to 50% of its blood volume, thus adding to venous return, cardiac output and HBF. Also activated immediately upon reduction of PF are the hepatic arterial buffer response and an HBF-dependent hepatorenal reflex. Adenosine is secreted at a constant rate into the small fluid space of Mall which surrounds the terminal branches of the hepatic arterioles, portal venules and sensory nerves. The concentration of adenosine is regulated by washout into the portal venules. Reduced PFreduces the washout and the accumulated adenosine causes dilation of the hepatic artery, thus buffering the PF change. Adenosine also activates hepatic sensory nerves to cause reflex renal fluid retention, thus increasing circulating blood volume and maintaining cardiac output and PF. If these mechanisms are not able to maintain total HBF, the hemodynamic imbalance results in hepatocyte proliferation, or apoptosis, by a shear stress/nitric oxide-dependent mechanism, to adjust total liver mass to match the blood supply. These mechanisms are specific to this unique vascular bed and provide an excellent example of multiple integrative regulation of a major homeostatic organ.     

Effects of vasopressin on haemodynamics in portal hypertensive rats receiving clonidine

Abstract: The effects of clonidine, vasopressin or a combination of both substances on splanchnic and systemic haemodynamics were measured in conscious rats with portal vein stenosis. Clonidine alone significantly decreased portal pressure, portal tributary blood flow and cardiac index, but did not change arterial pressure. Vasopressin alone significantly increased arterial pressure and significantly decreased portal pressure, portal tributary blood flow and cardiac index. Changes in portal tributary blood flow, arterial pressure and cardiac index were significantly higher with vasopressin than with clonidine alone. Vasopressin infusion in rats pretreated with clonidine significantly increased arterial pressure and significantly decreased portal pressure, portal tributary blood flow and cardiac index. Changes in arterial and portal pressures and portal tributary blood flow were significantly higher with combined therapy than with clonidine alone. Changes in arterial and portal pressures and portal tributary blood flow did not differ between combined therapy and vasopressin alone. Changes in cardiac index were significantly higher with combined therapy than with clonidine or vasopressin alone. Hepatic artery blood flow was not affected by either clonidine or vasopressin but significantly declined with combined therapy. In conclusion, this study suggests that a combination of vasopressin and clonidine accentuates the portal hypotensive action of clonidine but not the action of vasopressin. Moreover, this study suggests that a combination of vasopressin and clonidine may have deleterious effects on systemic and hepatic artery vascular beds.     

Role of hepatic artery in haemodynamics in normal and cirrhotic livers in rats

To examine the degree of influence of the hepatic artery on microcirculation in the liver, microscopic observation of blood flow in the hepatic minute blood vessels and the sinusoids and pressure measurements at key points in hepatic vascular pathways in vivo were performed before and after hepatic artery ligation in normal and cirrhotic rats. In normal rats, portal vein pressure (109 mmH2O) fell 10 mmH2O after hepatic artery ligation, but the pressures of the terminal portal venule, the terminal hepatic venule and the inferior vena cava did not change. In cirrhotic rats, portal vein pressure (206 mmH2O) and terminal portal venule pressure (106 mmH2O) fell 23 and 10 mmH2O after hepatic artery ligation respectively: the pressures in the terminal hepatic venule and the inferior vena cava did not change. These results suggests that the pressure transmitted from the hepatic artery was mostly supplied to the intrahepatic portal vein in normal rats and both to the intrahepatic portal vein and to the sinusoids in cirrhotic rats. In both normal and cirrhotic rats, however, the pressure transmitted from the hepatic artery was about 10 per cent of the initial portal vein pressure, and the blood flow in minute vessels and sinusoids did not change after hepatic artery ligation. Accordingly, it is believed that the hepatic artery plays only a small role in the haemodynamics of the liver in both normal and cirrhotic rats, irrespective of the distribution and manner of the hepatic arterial termination.