Importance of nitric oxide in hepatic arterial blood flow and total hepatic blood volume regulation in pigs

The importance of nitric oxide in regulating basal arterial blood flow has been examined in several different vascular beds by intra-arterial infusion of inhibitors of nitric oxide synthesis, but not in the arterial vascular bed of the liver. In the present study, N^G-nitro-L -arginine (L -NNA), in a dose of 0.5 and 1.0 μmol mL^?1 of hepatic arterial blood flow, was infused for 5 min into the hepatic artery in seven pigs anaesthetized with pentobarbital sodium. The haemodynamic effects observed by the first infusion were not further enhanced by the second infusion. Hepatic arterial resistance increased by 143 ± 38% and hepatic arterial blood flow declined by 38 ± 10%. A systemic effect due to `spillover' was observed, as evidenced by an increase in mean aortic blood pressure of 24 ± 4 mmHg. However, no significant increase in arterial mesenteric resistance was observed and total liver blood flow remained unchanged. Hepatic arterial vasodilation in response to occlusion of the portal vein, the arterial buffer response, remained intact after inhibition of nitric oxide synthesis. Liver lobe thickness, measured by an ultrasonic technique,was not found to change with inhibition of arterial nitric oxide synthesis, excluding a significant direct effect of arterial nitric oxide on liver capacitance. In conclusion, nitric oxide is an important regulator of hepatic arterial resistance, but does not mediate the hepatic arterial buffer response and was not found to play any significant role in total hepatic capacitance regulation.     

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.     

The effects of stimulation of the hepatic nerves, infusions of noradrenaline and occlusion of the carotid arteries on liver blood flow in the anaesthetized cat

1. In anaesthetized cats, the hepatic artery, portal vein and inferior vena cava pressures and the hepatic artery and portal vein flows were recorded using pressure transducers and electro-magnetic flowmeters.

2. The hepatic nerves were stimulated with maximal stimuli for periods of 2-5 min. The magnitude of the response varied with the frequency of stimulation over the range 1-10 impulses/sec. The resistance to flow increased in both the hepatic artery and the portal vein.

3. In the hepatic artery, mean pressure remained virtually constant, while the flow showed an initial marked decrease followed by a return towards the control level. In the portal vein, the flow remained constant while portal pressure showed a maintained increase. These responses were unaffected by previous administration of atropine and propranolol, but were blocked by phenoxybenzamine.

4. Infusions of noradrenaline into the hepatic artery produced changes similar to those following stimulation of the nerves. In contrast, when the hepatic arterial pressure was maintained constant, intravenous infusions of noradrenaline produced a maintained decrease in hepatic artery flow.

5. The occurrence of autoregulation of the hepatic artery flow at arterial pressures above 80-100 mm Hg was confirmed.

6. Occlusion of the carotid arteries caused a rise in arterial pressure with little change in hepatic artery flow, but when the hepatic artery pressure was maintained at the pre-occlusion level the flow showed an abrupt decrease, usually followed by a recovery towards the control level. This decrease was abolished by section of the hepatic nerves and removal of the adrenal glands.

7. It is concluded that the increase in hepatic artery resistance during occlusion of the carotid arteries was dependent on the hepatic nerves, the adrenal medullary secretions and an intrinsic autoregulatory mechanism.

     

正常肝脏汇管区微血管的分布和走行——哺乳动物肝脏微血管形态学研究Ⅲ

正常肝脏汇管区微血管的分布和走行——哺乳动物肝脏微血管形态学研究Ⅲ张俊杰＊刘丽莉＊王树哲我们研究小鼠、大白鼠和家兔肝脏汇管区内微血管的分布和走行，目的是从不同侧面加深对肝脏的生理功能及病理改变的理解。１材料与方法动物：小鼠７只，大白鼠７只，家兔５只。...     

Non-invasive measurement of hepatic oxygenation by an oxygen electrode in human orthotopic liver transplantation

Precise evaluation of graft reperfusion is difficult in clinical liver transplantation. The oxygen electrode (OE) is a novel technique to detect blood flow indirectly by measuring the quantity of oxygen which can diffuse from the hepatic tissue to the surface electrode. Application of the surface OE does not influence the liver blood flow or parenchymal perfusion. Adequate graft oxygenation is essential to the outcome of organ transplantation and has not previously been analysed intra-operatively in liver transplant recipients. The OE was applied to the surface of the graft intra-operatively in 22 human liver grafts after restoring portal vein and hepatic artery inflow. OE readings were compared with liver blood flow using an electromagnetic flowmeter (EMF). Intra-operative haemodynamics and donor organ parameters known to influence graft function were correlated with the OE readings. There was a significant correlation (r=0.89; p<0.001, n=14) between tissue oxygenation using the OE and total liver blood flow measured by EMF. The tissue oxygenation measurements were reproducible with a coefficient of variation of 5%. The hepatic tissue oxygenation increased significantly from baseline following venous reperfusion of the graft (282+/-23 vs 3107+/-288 (+/-SE) nA, p<0.001). Hepatic arterial revascularisation resulted in a significant (p<0.001) increase of 41+/-7% in liver oxygen perfusion. There was significant negative correlation (r=0.80, p<0.001, n=22) between cold ischaemic time and graft tissue oxygenation. The OE provides a reliable, cheap and non-invasive method of monitoring liver graft oxygenation and perfusion during transplantation.     

Control of hepatic and intestinal blood flow: effect of isovolaemic haemodilution on blood flow and oxygen uptake in the intact liver and intestines.

1. Limited isovolaemic haemodilution was produced in cats by addition of dextran 75-Ringer solution to an extracorporeal blood reservoir connected in series with the cat. Total hepatic venous outflow was neasured using a hepatic venous long-circuit and hepatic arterial flow was measured with an electromagnetic flow probe. Oxygen uptake was monitored in the guts and liver. Na-pentobarbitone anaesthesia was used. 2. Following reduction of the haematocrit (from 31 to 22) the oxygen uptake of the gut segment and liver were maintained. Gut conductance increased to 125% of control while the oxygen extraction ratio increased to only 109%. The hepatic arterial conductance did not change in spite of a greatly reduced (to 68%) oxygen delivery. Hepatic extraction increased to 140% of control. 3. The hepatic artery did not dilate to maintain constant oxygen supply to the liver thus confirming our previous observation that blood flow is not coupled to hepatic metabolism. 4. Oxygen extraction in the gut correlated well with changes in portal blood flow but not with changes in vascular conductance, arterial blood pressure or oxygen delivery. 5. The blood flow of the gut (vascular beds draining into the portal vein in the splenectomized preparation) was controlled in a manner that prevented changes in portal venous PO2 in spite of a reduction in oxygen content. Local PO2 and perhaps pH, are suggested as the factors controlling gut blood flow following haemodilution. 6. Changes in portal blood flow correlated with changes in portal vascular (intrahepatic) conductance such that increased portal flow produced an increased portal conductance thereby maintaining portal venous pressure constant.     

Intrahepatic distribution of portal and hepatic arterial blood flows in anaesthetized cats and dogs and the effects of portal occlusion, raised venous pressure and histamine

1. Radioactive microspheres were used to determine the distribution of arterial and portal flows within the liver. (141)Ce-microspheres and (51)Cr-spheres were given to allow two determinations of flow distribution in each animal and experiments are described to establish the accuracy and validity of the method.2. Mean flow/g to any lobe or segment of a lobe in a group of animals was not markedly different from the mean flow/g to the whole liver, and in general the liver was homogeneously perfused with both portal and arterial blood. However, in any one liver, some areas received a relatively greater flow (up to 300%) and some a relatively smaller flow (down to 50%) at the time the microspheres were given. The gall bladder received a much smaller portal flow/g than the parenchyma but its arterial flow/g varied widely in different animals.3. If portal flow to an area of parenchyma was reduced by occlusion of a branch of the portal vein, this area received a significantly increased arterial flow.4. An increase in hepatic venous pressure did not cause a significant change in the intrahepatic distribution of either arterial or portal flows in cats.5. In dogs, infusions of histamine into the portal vein caused a redistribution of portal flow away from the free ends of the lobes towards the hilar ends but the distribution between lobes did not change and there was no redistribution of arterial flow.     

Die Wirkung von Noradrenalin,Adrenalin, Isoproterenol und Adenosin auf die Durchblutung der Leber und des Splanchnicusgebietes des Hundes

Zusammenfassung In Chloralose-Urethan-Morphin-Narkose wurde an Hunden die Durchblutung der Arteria hepatica und der Vena portae mit elektromagnetischen Flowmetern gemessen. Die Wirkung von Dauerinfusionen kleiner Mengen Noradrenalin, Adrenalin, Isoproterenol und Adenosin auf die Leberdurchblutung wurde untersucht. Durch Infusion der Substanzen in eine periphere Vene, in die Arteria mesenterica cranialis, in die Vena portae und in die Arteria hepatica konnten die Wirkungen in solche auf die Mesenterialgefäße, die Vena portae und die Arteria hepatica getrennt werden.Im Mittel betrug die Pfortaderdurchblutung 500±34 ml/min und die Durchblutung der Arterie 105±12 ml/min. Bezogen auf 100 g Leberfeuchtgewicht betrug der Wert für die Pfortader 102,3±8,2 ml/min·100 g und für die Leberarterie 22,5±2,3 ml/min·100 g. Bezogen auf kg Körpergewicht lagen die Werte für die Pfortader bei 20,7 ml/min·kg und für die Arterie bei 4,3 ml/min·kg.Intravenös infundiert führte Noradrenalin zu einer Constriction der Mesenterialgefäße und damit zu einer Abnahme der Pfortaderdurchblutung und des Pfortaderdruckes. Adrenalin, Isoproterenol und Adenosin erhöhten die Pfortaderdurchblutung und den Pfortaderdruck durch Dilatation der Mesenterialgefäße. Die Wirkung auf die Arteria hepatica war bei i.v. Dauerinfusion kleiner Mengen ohne Bedeutung.Die Infusion von Noradrenalin oder Adrenalin entweder in die Arteria hepatica oder aber in die Vena portae führte zu einer Constriction der Arterie mit Minderung des arteriellen Einstromes, wobei die Wirkung auf die Arterie, ausgelöst von der venösen Seite her ebenso stark war wie die Wirkung, ausgelöst von der arteriellen Seite her.Isoproterenol und Adenosin dilatierten die Arteria hepatica unabhängig davon, ob sie über die Arterie oder über die Pfortader infundiert wurden. Die durch Isoproterenol verursachte Dilatation der Arterie konnte durch Inderal^® vollständig geblockt werden. Die Befunde über die Wirkung von Isoproterenol an der Leberarterie berechtigen zu der Annahme, daß es im Bett der Leberarterie ß-Receptoren gibt, und daß ein adrenergischer Dilatationsmechanismus existiert.Die starke Wirkung der untersuchten vasoaktiven Substanzen auf die Durchblutung der Arteria hepatica bei Infusion in die Vena portae läßt an eine größere physiologische Bedeutung der von Elias beschriebenen arteriellen Sphincter denken.An der intakten Leber kann die Größe der arteriellen Durchblutung reziprok durch die Größe der venösen Durchblutung beeinflußt werden.

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Summary The blood flow of the portal vein and the hepatic artery was measured in dogs in chloralose-urethan-morphin anesthesia with electromagnetic flowmeters. The effects of small amounts of norepinephrine, epinephrine, isoproterenol and adenosine on liver blood flow were studied. Infusion of these substances in a peripheral vein, in the cranial mesenteric artery, in the portal vein and in the hepatic artery allowed to differentiate between effects on the mesenteric vessels, on the portal vein and on the hepatic artery.The mean value of the portal flow was 500±34 ml/min and of the hepatic artery flow 105±12 ml/min. Related to 100 g liver wet weight the portal flow was 102.3±8.2 ml/min·100 g and the hepatic artery flow 22.5±2.3 ml/min·100 g. Related to kg body weight the portal flow was 20.7 ml/min·kg and the hepatic artery flow 4.3 ml/min·kg.Intravenous infusion of norepinephrine caused a constriction of the mesenteric vessels which was followed by a decrease of portal blood flow and portal pressure. Epinephrine, isoproterenol, and adenosine increased portal blood flow and portal pressure by dilatation of the mesenteric vessels. The effect of an intravenous infusion of small amounts of these substances on hepatic artery blood flow was negligible.The infusion of norepinephrine or epinephrine either in the hepatic artery or in the portal vein caused constriction of the hepatic artery with reduction of arterial inflow. The effect on the arterial inflow, produced by infusion in the portal vein was as strong as the effect produced by infusion in the hepatic artery.Isoproterenol and adenosine dilated the hepatic artery independent from the mode of application: Infusions in the portal vein and in the hepatic artery had the same effect. The dilatation, caused by isoproterenol could be completely blocked by Inderal^®. The findings of the action of isoproterenol on arterial inflow give reason to believe, that there are ß-receptors in the hepatic artery bed and that an adrenergic dilating mechanism exists.The strong effects of the substances on arterial blood flow, while infused in the portal vein allow to think of a greater physiological importance of the arterial sphincters, described by Ellas.In the intact liver the magnitude of the arterial inflow can be influenced reciprocally by the magnitude of the portal inflow.

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Mit Unterstützung der Deutschen Forschungsgemeinschaft.

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Stipendiat der Alexander von Humboldt-Stiftung.     

Effect of acid-base alterations on hepatic lactate utilization

1. The effect of acid-base changes on hepatic lactate utilization was investigated in anaesthetized, mechanically ventilated dogs.2. Portal vein flow and hepatic artery flow were measured with electromagnetic flowmeters, lactate concentration of portal vein, arterial and mixed hepatic venous blood was determined by an enzymatic technique, and hepatic lactate uptake was calculated using the Fick principle.3. Respiratory alkalosis (Delta pH 0.25 +/- 0.02) in four dogs resulted in a significant fall in total hepatic blood flow (-22 +/- 4%) and a significant rise in both arterial lactate concentration (2.18 +/- 0.32 m-mole/l.) and hepatic lactate utilization (3.9 +/- 1.2 mumole/min.kg).4. 0.6 M-Tris buffer infusion (Delta pH 0.21 +/- 0.02) in four dogs produced no significant changes in liver blood flow, arterial lactate concentration or hepatic lactate uptake.5. Respiratory acidosis (Delta pH -0.20 +/- 0.03) in six dogs and metabolic acidosis (Delta pH -0.20 +/- 0.02) in four dogs produced no significant changes in liver blood flow, decreases in arterial lactate concentration of 0.38 +/- 0.09 m-mole/l. (P < 0.05) and 0.13 +/- 0.13 m-mole/l., respectively, and no significant changes in hepatic lactate uptake.6. A significant correlation (r = 0.63; P < 0.01) was found between hepatic lactate utilization and arterial lactate concentration during the hyperlactataemia associated with respiratory alkalosis.7. Hyperlactataemia induced in four dogs by infusion of buffered sodium lactate (Delta pH 0.05 +/- 0.01;% Delta liver blood flow 29 +/- 7%) was also significantly correlated with hepatic lactate utilization (r = 0.70; P < 0.01) and the slope of the regression was similar to that during respiratory alkalosis.8. These data suggest that the hyperlactataemia of alkalosis is not due to impaired hepatic utilization of lactate and that the principal determinant of hepatic lactate uptake during alkalosis or lactate infusion is blood lactate concentration, rather than liver blood flow or acid-base status.     

Anatomy of hepatic arteriolo‐portal venular shunts evaluated by 3D micro‐CT imaging

The liver differs from other organs in that two vascular systems deliver its blood – the hepatic artery and the portal vein. However, how the two systems interact is not fully understood. We therefore studied the microvascular geometry of rat liver hepatic artery and portal vein injected with the contrast polymer Microfil^®. Intact isolated rat livers were imaged by micro‐CT and anatomic evidence for hepatic arteriolo‐portal venular shunts occurring between hepatic artery and portal vein branches was found. Simulations were performed to rule out the possibility of the observed shunts being artifacts resulting from image blurring. In addition, in the case of specimens where only the portal vein was injected, only the portal vein was opacified, whereas in hepatic artery injections, both the hepatic artery and portal vein were opacified. We conclude that mixing of the hepatic artery and portal vein blood can occur proximal to the sinusoidal level, and that the hepatic arteriolo‐portal venular shunts may function as a one‐way valve‐like mechanism, allowing flow only from the hepatic artery to the portal vein (and not the other way around).     

Direct effects of various catecholamines on liver circulation in dogs.

As measured by electromagnetic blood flow transducers, direct infusion of epinephrine, norepinephrine, and dopamine into the portal vein (PV) produced a 40-50% decrease in hepatic arterial (HA) blood flow; isoproterenol increased HA flow by about 69%. No changes in PV flow or pressure were observed. Direct HA infusion of the vasoconstrictors decreased HA flow by amounts comparable to those occurring after PV infusion. However, HA infusion of isoproterenol increased HA flow only 15% suggesting a difference in beta-receptor population in the two vessels. When infused directly into the superior mesenteric artery (SMA), epinephrine and norepinephrine reduced SMA flow by about 45% and PV flow by 20-25%; HA flow increased 6-8%. Infusion of isoproterenol and dopamine into SMA increased SMA flow by 115% and 206% and PV flow by 60% and 70%, respectively, whereas HA flow decreased by 25% and 50%. Portal vein pressure increased less than 3 mmHg. Alpha- and beta-receptor blockade of the liver did not change significantly the alterations in hepatic arterial blood flow that were secondary to changes in portal venous blood flow. It is likely that regulation of hepatic arterial flow resides in mechanisms located within the liver sinusoids.     

The effect of haemorrhage on hepatic artery and portal vein flows in the anesthetized cat

1. In cats anaesthetized with pentobarbitone, the hepatic artery and portal vein flows and pressures were recorded simultaneously.

2. Removal of blood from the animal did not cause a decrease in the hepatic artery flow unless the arterial pressure fell below 80 mm Hg. In contrast, the portal vein flow fell markedly.

3. After restoration of the blood, the hepatic artery flow increased to above the pre-haemorrhage level, while portal vein flow returned only partly towards the control level.

4. It is concluded that haemorrhage causes a vasodilation in the hepatic artery vascular bed and a vasoconstriction in the vascular beds drained by the portal vein. By this means, the oxygen supply to the liver is maintained as far as possible.

     

Hepatic outflow obstruction created by balloon occlusion of the hepatic vein: induced hepatic hemodynamic changes and the therapeutic applications of hepatic venous occlusion with a balloon catheter in interventional radiology

Hepatic outflow obstruction created by balloon occlusion of the hepatic vein induces characteristic angiographic findings in the occluded area: prolonged enhancement on hepatogram followed by reversed portal opacification on the hepatic arteriogram and perfusion defect on the arterial portogram. The following induced hepatic hemodynamic changes are suggested: hepatic arterial flow increases, and the portal vein acts as a draining vein with slow reversed flow. These unique hemodynamic changes enhance the effect of hepatic interventional therapies. In transcatheter arterial infusion, increasing hepatic arterial flow and absence of portal inflow can bring about a high concentration of drugs, the presence of which is greatly protracted due to outflow blockage. In transcatheter arterial chemoembolization, reversed portal flow can allow portal embolization in addition to arterial embolization. In microwave coagulation therapy and radiofrequency ablation therapy, decreasing portal flow can cause larger areas of coagulation. Further, the technique of hepatic venous occlusion has potential therapeutic applications.     

大鼠"二袖套"法双重灌注全血供肝移植模型的建立

目的：建立一个供肝灌注良好受体无肝期明显缩短及移植肝全血供稳定的肝移植动物模型。方法：“二袖套”法在Kamada吻合血管基础上改良,供肝分别经腹主动脉和门静脉双重全肝脏灌注;受体肝脏分步切除,肝上下腔静脉采用缝合法吻合,门静脉和肝下下腔静脉分别用袖套法吻合。移植肝脏动脉重建采用单纯血管套入式吻合或血管缝合的方法,胆总管采用单管内支架胆管端端吻合法。结果：共施行全血供大鼠原位肝脏移植76例（不包括预试验）,手术成功率93．406,1周存活率86．8％。结论：娴熟的显微外科技术、有效改良措施和注重手术细节是手术成功的保障,良好的灌注、受体无肝期的缩短及重建移植肝脏动脉血供能有效提高动物模型的稳定性。     

Meal induced changes in hepatic and splanchnic circulation: a noninvasive Doppler study in normal humans

Summary The haemodynamic effects of a meal on the splanchnic and hepatic circulation were evaluated in 30 healthy volunteers, using Doppler ultrasonography. The resistance index (RI) of the superior mesenteric artery and of the left and right intrahepatic arteries, the portal vein blood flow as well as the ratio between maximal velocity in the left and right intrahepatic arteries and the adjacent portal vein were measured initially, then 15, 30, 45, and 60 min after the ingestion of a standard balanced liquid meal. Postprandial haemodynamic changes were maximal 30 min after the meal; at that time, mesenteric artery RI decreased significantly [mean –11% (SEM 14%)] whereas portal vein blood flow increased markedly [mean +79% (SEM 14%)]; a significant increase in hepatic artery RI was observed in both liver lobes. The ratio between maximal velocities of the intrahepatic artery and the intrahepatic portal vein was reduced significantly; this ratio decreased more markedly in the right lobe of the liver. These findings would suggest that there was an adaptation of hepatic artery to portal vein blood flow after a meal. The subsequent increase in intrahepatic portal vein flow velocity was found to be greater in the right lobe of the liver.     

Ermittlung ventrikulärer Druck-Geschwindigkeitskurven unter Berücksichtigung des enddiastolischen Druckes

Summary The effects of intravenous, intra-arterial and intraportal administration of glucagon on hepatic artery and portal vein flows were studied in anaesthetized dogs. Intravenous administration of glucagon (10 g/kg) increased hepatic arterial and portal venous flows by 155% and 176% of the control value respectively. Intraarterial injection of glucagon increased hepatic artery flow and decreased its resistance. The hepatic arterial effect of glucagon was dose-dependent and was not abolished after -adrenoceptor blockade by propranolol 1 mg/kg i.v., or after denervation. Intraportal injection of glucagon had no direct immediate (<15 sec) effect on portal venous flow or pressure. This was followed by an increase in portal vein flow and pressure reaching maximal response within 3–5 min. This late effect was most likely the result of the mesenteric vasodilator action of glucagon. It is concluded that glucagon posses a direct dilator action on the hepatic artery, and indirectly influences the portal venous circulation. Glucagon may have a physiological role in the hepatic vascular bed.This study was supported by NIH Grants HE-07739 and HL-05396 and Cardiology Research and Teaching Fund.Preliminary Communication of this work was presented at the Fall Meeting of the American Physiological Society, 16.–19. August 1971, and appeared as abstract in the Physiologist14, 108 (1971).     

Hepatic arterial perfusion regulates portal venous flow between hepatic sinusoids and intrahepatic shunts in the normal rat liver in vitro

Intrahepatic shunts regulate portal venous pressure during periods of acute portal hypertension when the transhepatic portal resistance is momentarily increased in the normal rat liver in vivo. Hepatic arterial inflow may also increase the transhepatic portal resistance and activate intrahepatic shunts. In the present study, the transhepatic portal resistance and the activity of intra-hepatic shunts were measured in vitro and the point of confluence between the hepatic artery and portal vein in the rat determined. Livers of male Sprague-Dawley rats were single-pass, dual-perfused in vitro. Total cessation or diversion of the hepatic arterial inflow to the portal venous vasculature, whilst maintaining total hepatic perfusate flow, decreased intrasinusoidal pressure, increased transhepatic portal venous resistance and opened the portal venous intrahepatic shunts in a manner similar to intraportal injection of 15-microm diameter microspheres. Injections of the microspheres into the hepatic arterial circulation increased hepatic arterial pressure dramatically, consistent with complete occlusion of the arterial vasculature. The intrahepatic shunts are located at a pre-sinusoidal level because no increases were detected in hepatic arterial pressure following intraportal injection of microspheres. The hepatic arterial vasculature, unlike the portal supply, does not possess a collateral shunt circulation and coalesces with the portal vein at an intrasinusoidal location     

The hepatic haemodynamic response to acute portal venous blood flow reductions in the dog

The hepatic haemodynamic response to acute reductions in portal venous blood flow was investigated in 14 anaesthetized normal dogs. A side-to-side mesocaval anastomosis was constructed to enable varying degrees of portal flow to be diverted into the inferior vena cava by suitable manipulations of the shunt diameter. Measurements of portal venous and hepatic arterial blood flow were made with electromagnetic flowmeters.A linear relationship was observed between the degree of reduction in portal flow and the magnitude of the resulting hepatic arterial hyperaemic response. Hepatic arterial vascular resistance showed a decrease which became more pronounced the greater the degree of reduction in portal flow. For every 1.0 ml·min^–1 100 g^–1 decrease in portal flow, the hepatic arterial flow increased by a mean of 0.24 ml ·min^–1·100g^–1, a value representing the average compensatory capacity of the arterial response. Arterial flow improvement therefore provided some degree of protection against severe falls in total liver blood flow. However, it provided even more effective protection against any fall in total hepatic oxygen consumption, which showed only a very gradual decrease with reduced hepatic portal blood flow.     

Effect of Substance P on Various Vascular Beds in the Dog

Using the electromagnetic flowmeter technique, the blood flow in the aorta, carotid, hepatic, superior mesenteric, renal and femoral arteries and portal vein was recorded during continuous i.v. infusion of synthetic Substance P (SP) in 8 dogs. Systemic and portal blood pressures were recorded. A significant decrease in mean arterial blood pressure was recorded at infusion of SP in the femoral vein at a rate of 2.5 ng × min^-1× kg b.w.^-1 or higher. Portal venous blood pressure increased. A rapid increase in the carotid, hepatic, mesenteric and portal blood flow was obtained at infusion rates of 1.2 ng × min^-1× kg b.w.^-1 or higher. The femoral artery responded with a late, transient increase in flow, with a return to the base level while the infusion was still in progress. The renal artery blood flow decreased slightly at low infusion rates and increased at higher. At SP infusions in the portal vein the infusion rate had to be increased to 20 ng × min^-1× kg b.w.^-1 or higher before any general vascular reactions were recorded, indicating that the liver has a high capacity for inactivating SP.     

Early graft hemodynamics in living related liver transplantation evaluated by Doppler ultrasonography

The aim of this study was to clarify the perioperative hemodynamics of liver grafts without vascular complications during and early after liver transplantation from living donors. This study was carried out in 4 child recipients (lateral segment left lobe grafts) and 6 adult recipients (right lobe grafts) of liver transplantation from living donors. The hemodynamics of the hepatic artery, portal vein, and hepatic vein of the grafts during and until 7 days after surgery were studied by Doppler ultrasonography. The maximum flow velocity of the hepatic artery, mean portal blood flow velocity, and pulsatility index (PI) of the hepatic artery increased in all 10 grafts with no vascular complication after vascular anastomosis. After surgery, the mean portal blood flow velocity showed a peak 3 days after surgery and reached a nadir 7 days after surgery in both the lateral segment left lobe grafts in children and the right lobe grafts in adults, but it was significantly higher in the right lobe grafts in adults (mean +/- SD 31.0 +/- 6.3 vs. 22.4 +/- 0.9 cm/sec). Also, as the hepatic artery blood flow velocity increased the portal blood flow velocity decreased, the hepatic blood flow during liver regeneration was suggested to be controlled by both the artery and portal vein. The range of PI of the hepatic artery was 0.60-1.86. The mean hepatic venous blood flow was stable throughout the observation period (30.4 +/- 8.8 cm/sec). Although the hepatic venous flow waves changed widely from pulsed waves to a flat flow, its changes did not suggest a vascular complication. Evaluation of changes by Doppler ultrasonography in the hemodynamics of the liver grafts without vascular complications during and early after liver transplantation from living donors is considered to be useful for accurate monitoring of the hemodynamics during liver regeneration and early detection of abnormalities.