Hepatic Arterial Blood Flow Research Articles

Hepatic effects of influxed endothelin-1 from portal vein: in situ portal vein infusion model using dogs

Endothelin-1 is a potent vasoconstrictor formed by vascular endothelium. This study was designed to investigate the hepatic effect of endothelin-1 produced by portal vascular endothelium. Portal venous pressure, portal venous flow, hepatic arterial flow, tissue blood flow, and tissue oxygen pressure were measured during portal vein endothelin-1 infusion in dogs at rates of 1.0 to 5.0 ng/kg per minute. Sinusoidal width during maximal infusion was determined morphometrically. Serum concentrations of mitochondrial glutamic oxaloacetic transaminase and endothelin-1 in portal and hepatic venous blood were also measured. Intraportal endothelin-1 infusion dose-dependently increased portal venous pressure and reduced portal venous and hepatic arterial blood flow. Tissue blood flow and oxygen pressure also decreased. Endothelin-1 also significantly increased serum mitochondrial glutamic oxaloacetic transaminase and constricted hepatic sinusoids. These changes reversed after completion of infusion. Intraportal endothelin-1 caused circulatory and histological changes in hepatic sinusoids that may suggest the role of endothelin-1 formed by portal venous bed epithelium.

Transarterial Chemoembolization With Degradable Starch Microspheres, Irinotecan, and Mitomycin-C in Patients With Liver Metastases

Degradable starch microspheres (DSMs) provide transient occlusion of small arteries and are thought to improve the therapeutic effect of anticancer drugs. Irinotecan (CPT-11) is one of the most effective anticancer agents. We herein report cases with liver metastases treated with transarterial chemoembolization with DSM, CPT-11, and mitomycin-C (DSM-CPT therapy). Five patients underwent DSM-CPT therapy for liver metastases that originated from colorectal cancer for four and gastric cancer for one. They all lack indication for surgery. They were all male with an age range of 42-78 years (mean, 55.2 years). Three of them had pretreatment histories with 5-fluorouracil or related agents, and four of them had combined systemic or local chemotherapy at the period. Required doses for stasis of whole blood flow of hepatic artery of DSMs were used with CPT-11 and mitomycin-C. After one to six injections, four patients had a partial response and the disease progressed in one patient with gastric cancer origin. Two of the partial response patients underwent surgery after 2 months of the partial response period. Carcinoembryonic antigen and CA19-9 levels in partial response patients decreased to 16.1% and 19.3% of the level before treatment, respectively. DSM-CPT therapy can be a potential therapy for liver metastases.

The Effect of Vasopressin on Organ Blood Flow in an Endotoxin-Induced Rabbit Shock Model

The effects of vasopressin on the vasculature differ from those of other vasopressors, and its effects on the coronary artery remain debatable. This study was undertaken to examine the effects of vasopressin in a rabbit endotoxin-induced shock model and to compare these effects with those of norepinephrine. Thirty rabbits were divided into four study groups: a normal control group (group I, n = 5), a shock control group (group II, n = 5), a vasopressin group (group III, n = 10), and a norepinephrine group (group IV, n = 10). Shock was induced by intravenously infusing lipopolysaccharide (Escherichia coli O111:B4) in groups II, III, and IV. In groups III and IV, systemic blood pressure was maintained to the level of group I by adjusting vasopressin and norepinephrine doses. Left ventricle, right ventricle, ventricular septum, kidney, liver, spleen, and skeletal muscle blood flows were measured using radioisotope tagged microspheres at baseline and 2 h after initial blood flow measurement. No difference in organ blood flows were observed between groups I and II, and coronary blood flow in the left ventricle, right ventricle, and ventricular septum was similar in all study groups. However, renal blood flow was significantly lower in group IV than in group III (p <. 05) and hepatic arterial blood flow was significantly lower in group III than in group IV (p <. 05). Thus, effect of vasopressin on organ blood flow is organ dependent. Vasopressin increased renal blood flow and decreased hepatic arterial blood flow in this endotoxin-induced shock model, whereas norepinephrine did not. However, coronary blood flow was not changed by shock status or vasopressor type.

Intraoperative Blood Flow Measurements and Liver Allograft Function: Preliminary Results

Introduction Our previous studies showed a correlation of intraoperative renal allograft blood flow and immediate functions. A similar relation is not well established for liver transplantation. The aim of this study was to assess the relation between hepatic blood flow on revascularization and immediate liver graft function (IF). Methods Studies evaluating arterial and portal flow in newly transplanted livers were started in May 2004. Total hepatic artery and portal vein blood flow were assessed in 15 liver transplant recipients. Parenchymal flow was also recorded. Measurements were taken at 30 and 120 minutes after simultaneous arterial/portal reperfusion. Flow results were correlated with IF. Results Mean arterial blood flow (ABF) was 16.3 mL/min/100 g in both measurements. Portal flow was reduced from 168 to 127 mL/min/100 g from the first to the second measurement. Mean parenchymal flow (PF) did not alter over time (29.1 and 30.4 mL/min/100 g, respectively). Among recorded flow results we observed a significant correlation between PF with IF measured as: bile volume (R = 0.36 to 0.62; P < .05), serum AST (R = −0.4 to −0.68; P < .05), and ALT level (R = −0.2 to −0.71; P < .05), bilirubin level as well as INR (R = −0.39 to −0.61; P < .05) assayed daily for 14 days. Similar observations were made between ABF and INR, hiatal parenchymal flow, and ALT as well as INR. Conclusions These preliminary results suggest hepatic blood flow may be a reliable predictor of graft viability and function. Of the variables measured, portal blood flow seems to be the most valuable indicator of liver function.

IMPACT OF BLOOD FLOW OCCLUSION ON LIVER NECROSIS FOLLOWING THERMAL ABLATION

Laser, radiofrequency and microwave are common techniques for local destruction of liver tumours by thermal ablation. The main limitation of thermal ablation treatment is the volume of necrosis that can be achieved. Blood flow occlusion is commonly advocated as an adjunct to thermal ablation to increase the volume of tissue necrosis based on macroscopic and histological assessment of immediate or direct thermal injury. This study examines the impact of blood flow occlusion on direct and indirect laser induced thermal liver injury in a murine model using histochemical methods to assess tissue vitality. Thermal ablation produced by neodymium yttrium-aluminium-garnet laser (wavelength 1064 nm) was applied to the liver of inbred male CBA strain mice at 2 W for 50 s (100 J). Treatment was performed with and without temporary portal vein and hepatic artery blood flow occlusion. Animals were killed upon completion of the procedure to assess direct thermal injury or at 24, 48 and 72 h to assess the progression of tissue damage. The maximum diameter of necrosis was assessed by vital staining for nicotinamide adenine dinucleotide (NADH) diaphorase. Microvascular changes were assessed by laser Doppler flowmetry, confocal in vivo microscopy and scanning electron microscopy. The direct thermal injury (mean SE) assessed by NADH diaphorase staining was significantly greater following thermal ablation treatment without blood flow occlusion than with blood flow occlusion (3.3 (0.4) mm vs 2.9 (0.3) mm; P = 0.005). Tissue disruption, cracking and vacuolization was more pronounced adjacent to the fibre insertion site in the group treated with thermal ablation combined with blood flow occlusion. There was an equivalent increase in the extent of injury following therapy in both groups that reached a peak at 48 h. The maximum diameter of necrosis in the thermal ablation alone group at 48 h was significantly greater than the thermal ablation combined with blood flow occlusion group (5.8 (0.4) mm vs 5.3 (0.3) mm; P = 0.011). The patterns of microvascular injury were similar in both groups, varying in extent. Temporary blood flow inflow occlusion appears to decrease the extent of initial injury measured by vital staining techniques and does not alter the time sequence of progressive tissue injury following thermal ablation therapy.

Hepatic haemodynamic changes after portacaval anastomosis in normal, cirrhotic and chronic prehepatic portally hypertensive rats

Radioactive microspheres were used to determine the hepatic haemodynamic response to portacaval anastomosis in normal, cirrhotic and chronic prehepatic portally hypertensive rats 20 days after operation, and in normal rats 2 months after operation. After 20 days portacaval anastomosis caused a decrease in liver mass only in normal and cirrhotic animals, whereas hepatic arterial blood flow per unit of mass increased in normal (+488 per cent), cirrhotic (+191 per cent) and prehepatic portally hypertensive rats (+133 per cent). Despite these facts, animals with portacaval anastomosis showed a reduced hepatic total perfusion (arterial plus portal inflow) per unit of mass with respect to controls in normal (-53 per cent) and cirrhotic rats (-68 per cent), but not in those with prehepatic portal hypertension. Comparing studies carried out at 2 months with those performed 20 days after portacaval anastomosis in normal rats, some recovery of liver mass and total liver blood flow was observed. In conclusion, portacaval anastomosis produced a limited increase in hepatic arterial blood flow which was unable to preserve liver mass and its total perfusion in normal and cirrhotic animals. In contrast, portacaval anastomosis did not significantly alter liver mass or its perfusion in animals with chronic prehepatic portal hypertension, as both values were previously diminished in controls. Thus, the risk of liver failure after portacaval anastomosis is higher in normal and cirrhotic rats than in those with chronic prehepatic portal hypertension.

Ruptured hepatic artery aneurysm treated by saphenous vein graft.

Abstract The first recorded case in which a ruptured hepatic artery aneurysm has been treated with a saphenous vein graft replacement is presented. The indications for restoration of hepatic artery blood flow in patients with ruptured hepatic aneurysm are discussed.

Early detection of occult colorectal hepatic metastases using duplex colour Doppler sonography.

Previous studies have shown that overt intrahepatic tumours are associated with subtle changes in liver perfusion that can be measured directly using duplex colour Doppler sonography (DCDS). This study assessed the predictive value of DCDS in the early detection of occult colorectal hepatic metastases. Hepatic arterial and portal venous blood flow was measured in 50 control subjects and 135 patients with colorectal cancer, 67 with overt liver metastases and 68 with an apparently disease-free liver on the basis of computed tomography and laparotomy findings. The Doppler perfusion index (DPI), defined as the ratio of hepatic arterial to total liver blood flow, was calculated. Clear separation of the DPI values of controls and those of patients with overt metastases was observed (P < 0.0001). Thirty-eight of the 68 patients with a disease-free liver also had an abnormally high DPI value. After 1 year of follow-up, 21 patients with an abnormally high DPI at the time of apparently curative primary resection had developed liver metastases and a further four had died without post-mortem examination. The 30 patients with normal DPI remain disease-free. The data suggest that DPI is of value in the early detection of occult liver metastases.

Hepatic Arterial Buffer Response Fails to Restore Hepatic Oxygenation After Temporary Liver Dearterialization in Canines

Background Hepatic artery thrombosis is a rare but extremely troublesome condition after liver transplantation. Recently, urgent arterial revascularization has been used as rescue therapy, leading to improved graft and patient survivals. Hepatic artery ligation produces a progressive reduction in portal vein blood flow. Theoretically, a hyperemic response may be expected following hepatic artery reperfusion (hepatic artery buffer response, HABR). In this study, we tested the hypothesis that HABR can maintain adequate liver oxygenation after temporary liver dearterialization. Methods Seven dogs (19.7 ± 1.2 kg) subjected to 60 minutes of hepatic artery occlusion were observed for 120 minutes thereafter. Systemic hemodynamics was evaluated through Swan-Ganz and arterial catheters, and splanchnic perfusion by portal vein and hepatic artery blood flows (PVBF and HABF) via an ultrasonic flowprobe. Liver enzymes (ALT and LDH) and systemic and hepatic oxygen delivery (DO 2hepat) were calculated using standard formulae. Results Hepatic artery occlusion induced a progressive reduction in PVBF and DO 2hepat. A complete restoration of HABF after hepatic artery declamping was observed; however, the DO 2hepat (33.3 ± 5.9 to 16.5 ± 5.9 mL/min) did not return to the baseline levels. Conclusion Temporary hepatic artery occlusion induced a progressive decrease in portal vein blood flow during ischemia, an effect that continued during the reperfusion period. The hepatic artery blood flow was promptly restored after declamping. However, HABR was not able to restore hepatic oxygen delivery to baseline levels during the reperfusion period.

Continuous Transcatheter Arterial Thrombolysis for Early Hepatic Artery Thrombosis After Liver Transplantation

Early hepatic artery thrombosis (HAT) after orthotopic liver transplantation remains a significant cause of graft loss and patient death. The most effective treatment approach is still controversial. The purpose of this study was to assess the effect of continuous transcatheter arterial thrombolysis in the treatment of early HAT. Routine posttransplant color Doppler imaging (CDI) was performed to monitor hepatic artery blood flow. HAT was confirmed by arterial angiography in suspected cases. HAT was identified in 8 patients (8/287, 2.8%) which occurred on days 2 to 19 (mean, 5.2 days) after liver transplantation. Patients with HAT were treated with continuous transcatheter arterial thrombolysis using urokinase. Successful revascularization through thrombolysis was obtained in all eight cases. One patient died of a pulmonary infection at 2 months after liver transplantation. Another patient underwent retransplantation because of resistant allograft rejection and recurrence of HAT 6 months after the first operation, but died from multiple system organ failure 2 months later. The other six patients remained in good health during the follow-up period of 3 to 27 months. Our results demonstrate that CDI is an effective method to monitor the occurrence of early HAT after liver transplantation. Furthermore, continuous transcatheter arterial thrombolysis with urokinase could be a rational therapeutic approach to rescue the allograft following early HAT diagnosis confirmed by arterial angiography.

Hepatic hyperplastic nodules showing stains by portal blood flow: hemodynamics revealed by CTAP and CTHA

The hepatic hyperplastic nodule associated with idiopathic portal hypertension is classified as portal blood flow and hepatic arterial blood flow dominant types. These nodular lesions are considered attributable to abnormal blood flow in the liver. We describe a rare case of hepatic hyperplastic nodules showing stains by portal blood flow.

An alternative method of arterial reconstruction in pediatric living donor liver transplantation with the recipient right gastroepiploic artery

The classical method for arterial reconstruction in pediatric living donor liver transplantation using left lateral segment consists of end-to-end anastomosis between the donor left hepatic artery and the recipient right hepatic artery. In the present case, an intra-operative hepatic artery thrombosis occurred because of extensive intima wall dissection of the recipient hepatic artery. The patient was a 6-yr-old boy with fulminant hepatic failure, who underwent living donor partial liver transplantation with left lateral segment from his father. The graft was irrigated by a left hepatic artery and an accessory left hepatic artery from gastric artery, both arteries with diameter of <2 mm. These arteries were anastomosed to the recipient right and left hepatic arteries, respectively. Before performing the bile duct reconstruction it was noted that these anastomoses were occluded by clots of blood. An extensive subintimal dissection of the recipient hepatic artery was the cause of this problem. The creation of a new anastomosis by using a more proximal part of this artery without subintimal dissection was judged impossible. Then, the right gastroepiploic artery was mobilized and an anastomosis was performed with the donor left hepatic artery in an end-to-end fashion. Arterial blood flow to the graft was established successfully and the patient's postoperative recovery was excellent. Fifteen days after the transplantation, an angiotomography demonstrated a good hepatic arterial blood flow. The patient is now alive and well, 4 months after the transplantation. In conclusion, the method of hepatic graft arterialization described here is an important option for patients who undergo living donor or split liver transplantation.

New Measurement of Hepatic Blood Flow by Xenon CT System: An Animal Study with PGE1

A new Xenon computed tomography (CT) system was developed to measure both hepatic arterial and portal venous tissue blood flow (HATBF/PVTBF) non-invasively. Despite its clinical trial, the effect of prostaglandin E1 (PGE1) on hepatic hemodynamics is not well investigated. In a rabbit model, we evaluated the accuracy of this system by comparing it with the electromagnetic blood flowmeter (EMBF), the pharmacological effect of PGE1 on the fractional hepatic hemodynamics. Seven NZW-rabbits were used. Serial abdominal CT scan was obtained every min before and during the 4 min inhalation of the Xenon gas, followed by 5 min administration of oxygen air. From these images, HATBF and PVTBF were separately calculated with a special new imaging system. We also used EMBF during laparotomy, and directly measured the hepatic arterial and portal venous flow with or without PGE1 administration. Xenon CT showed HATBF of 18.4 +/- 4.5 (ml/min/100 g) and PVTBF of 69.4 +/- 15.0, was almost identical with those of EMBF (19.8 +/- 5.7 and 67.2 +/- 19.1, respectively). After PGE1 administration, Xenon CT showed 22.9 +/- 4.6 and 76.5 +/- 20.5, while those with EMBF were 21.0 +/- 6.5 and 84.7 +/- 21.6, respectively. There were significant correlations (P < 0.01) in total HTBF, HATBF, and PVTBF between results of Xenon CT and EMBF. Xenon CT with a newly developed imaging system enables us to measure the fractional hepatic tissue blood flow in rabbits, differentially and accurately. Venous administration of PGE1 increased total hepatic blood flow, mainly affecting the portal blood flow.

The role of nitric oxide in the modulation of hepatic microcirculation and tissue oxygenation in an experimental model of hepatic steatosis

Background: Impairment of hepatic microcirculation in fatty liver has been assumed to reduce tolerance of the liver against ischemia–reperfusion injury. The present study was aimed to investigate the role of nitric oxide (NO) in the regulation of hepatic microcirculation and tissue oxygenation in hepatic steatosis. Methods: Sprague–Dawley rats (200–250 g) were fed a 2% cholesterol diet ( n = 12) to induce hepatic steatosis or normal diet ( n = 12) served as controls for 12 weeks. Hepatic blood flow, microcirculation, tissue oxyhemoglobin (HbO 2) and cytochrome c oxidase radox status (Cyt Ox) in response to intravenous bolus administrations of l-arginine (300 mg/kg) or l-NAME (20 mg/kg) were assessed. Results: Animals which developed moderate hepatic steatosis showed significant increase in tissue level of total lipids. Portal blood flow and hepatic microcirculation were significantly reduced as compared to controls (5.7 ± 0.9 vs. 9.7 ± 0.9 ml/min, P = 0.003 and 114.5 ± 9.5 vs. 167.3 ± 10.0 flux unit, P = 0.003). l-Arginine improved hepatic arterial and portal blood flows as well as microcirculation in fatty livers ( P < 0.05), while l-NAME significantly worsened these parameters ( P < 0.05). Hepatic tissue HbO 2 and Cyt Ox were improved both in fatty and control livers following l-arginine, while l-NAME resulted in decreased HbO 2 and Cyt Ox although a transit increase in tissue oxygenation was observed in fatty livers. Conclusions: NO is involved in the modulation of hepatic microcirculatory perfusion and oxygenation in cholesterol-induced hepatic steatosis. NO metabolisms may be regulated as a potential therapeutic strategy for impaired microcirculation in hepatic steatosis.

Active Spleno-Femoral Shunt Avoids Splanchnic Congestion During Portal Triad Occlusion: An Experimental Study

Portal triad occlusion (PTO) is often performed during hepatic resections for trauma or malignancies to minimize intraoperative blood loss. The pringle maneuver is also regularly required during liver transplantation. This maneuver leads to temporary hepatic ischemia and may be associated with splanchnic blood flow congestion, promoting undesirable hemodynamic disturbances in some patients. Veno-venous bypass is a useful, easily performed technique that may avoid those deleterious hemodynamic effects of PTO. We tested the hypothesis that an active spleno-femoral shunt maintains hemodynamic stability and promotes complete decompression of the mesenteric bed, avoiding intestinal mucosal blood congestion, during PTO. Methods Seven dogs (17.2 ± 0.9 kg) were subjected to 45 minutes of hepatic ischemia during which there was an active spleno-femoral shunt. Systemic hemodynamics were evaluated through Swan-Ganz and arterial catheters. Splanchnic perfusion was assessed by portal vein blood flow and hepatic artery blood flow (PVBF and HABF, ultrasonic flowprobe), intestinal mucosal-arterial pCO 2 gradient (D t-apCO 2, tonometry), and regional O 2-derived variables. Results No significant changes in systemic and regional parameters were observed during the ischemia period. During reperfusion, a significant decrease in mean arterial pressure, PVBF, and arterial pH was observed. A significant increase in ALT and D t-apCO 2 (4.8 ± 2.5 to 18.9 ± 3 mm Hg) was also observed following hepatic blood flow restoration. Conclusion Spleno-femoral shunt maintains systemic hemodynamic stability, with an effective decompression of the splanchnic bed during portal triad occlusion. The deleterious hemodynamic and metabolic effects observed during reperfusion period, such as transitory hypotension, high D t-apCO 2, and acidemia, were associated with an isolated hepatic ischemia-reperfusion injury, not with the blood congestion in the splanchnic bed.

Radiofrequency Ablation for Hypersplenism in Patients With Liver Cirrhosis: A Pilot Study

Radiofrequency ablation is a relatively new technique used for local ablation of unresectable tumors. We investigated the feasibility and efficacy of radiofrequency ablation for hypersplenism and its effect on liver function in patients with liver cirrhosis and portal hypertension. Nine consecutive patients with hypersplenism due to cirrhotic portal hypertension underwent radiofrequency ablation in enlarged spleens. The ablation was performed either intraoperatively or percutaneously. Patients are followed up for over 12 months. After treatment, between 20% and 43% of spleen volume was ablated, and spleen volume increased by 4%-10.2%. White blood cell count, platelet count, liver function, and hepatic artery blood flow showed significant improvement after 1-year follow-up. Splenic vein and portal vein blood flow were significantly reduced. Only minor complications including hydrothorax (three of nine patients) and mild abdominal pain (four of nine patients) were observed. No mortality or other morbidity occurred. Radiofrequency ablation is a safe, effective, and minimally invasive approach for the management of splenomegaly and hypersplenism in patients with liver cirrhosis and portal hypertension. Increased hepatic artery blood flow may be responsible for sustained improvement of liver condition. Radiofrequency ablation may be used as a bridging therapy for cirrhotic patients waiting for liver transplantation.

Radiofrequency ablation for hypersplenism due to portal hypertension: clinical study

To investigate the feasibility, efficacy and clinical prospects of radiofrequency ablation (RFA) for hypersplenism in patients with liver cirrhosis and portal hypertension. The laboratory and radiologic data over one-year period of patients undergone splenic RFA were analyzed. Nine patients undergone splenic RFA has closely followed-up over 1 year. During hospitalization, no procedure-related complications occurred, only minor complications including hydrothorax (3/9 patients) and mild abdominal pain (4/9 patients) were observed. After treatment, average 30.7% (20%-43%) of spleen volume was ablated, and the platelet count reached peak on 14th post-procedure day. White blood cell and platelet counts, liver function, and hepatic artery blood flow had gained significant improvements comparing with those before RFA procedures. Hyperplasia/regeneration was also occurred in cirrhotic liver after splenic RFA. Radiofrequency ablation is a safe, effective and minimally invasive approach for the management of hypersplenism in patients with liver cirrhosis and portal hypertension. Increased hepatic artery blood flow can contribute to significant improvement of liver function, and maybe potentially stimulate liver regeneration in cirrhotic liver.

Physical hemodynamic interaction between portal venous and hepatic arterial blood flow in humans

The hepatic arterial end-diastolic velocity (HAEDV) is normally equal to portal vein peak velocity (PVPV). However, there is no report of quantitative measurement that HAEDV was equal to PVPV. We investigated the interaction in PVPV and HAEDV in both chronic and acute hepatic hemodynamic changes. One hundred and nineteen patients (54 with cirrhosis, 23 with chronic hepatitis, and 42 with no diffuse liver disorder) were enrolled. We investigated the differences in PVPV and HAEDV among the patients with and without liver disorder. In addition, we measured the intraindividual changes in HAEDV when PVPV was mechanically changed by percutaneous isolated hepatic perfusion in six patients and by percutaneous transhepatic portal embolization (PTPE) in six more. HAEDV was nearly equal to PVPV not only in patients with both normal and hepatitis but also in those with cirrhosis (PVPV-HAEDV = 3.0 +/- 5.2, 2.2 +/- 5.4, 2.3 +/- 6.5 cm/s, respectively). In the intraindividual study, both PVPV and HAEDV decreased during hepatic mechanical perfusion and HAEDV was equal to PVPV (8.2 +/- 2.8, 10.5 +/- 1.5 cm/s, respectively). After PTPE, PVPV was increased and hepatic arterial peak systolic velocity was reciprocally decreased. However, HAEDV was nearly equal to PVPV 7 days after PTPE (PVPV-HAEDV = 5.9 +/- 5.1 cm/s). Since arterial end-diastolic velocity depends on the downstream vascular resistance, lower HAEDV in patients with cirrhosis was considered to reflect a high outflow resistance. If there is no collateral pathway, we consider that HAEDV may actually reflect sinusoidal resistance to the same degree as PVPV.

Perfusion Imaging of the Liver: Current Challenges and Future Goals

Improved therapeutic options for hepatocellular carcinoma and metastatic disease place greater demands on diagnostic and surveillance tests for liver disease. Existing diagnostic imaging techniques provide limited evaluation of tissue characteristics beyond morphology; perfusion imaging of the liver has potential to improve this shortcoming. The ability to resolve hepatic arterial and portal venous components of blood flow on a global and regional basis constitutes the primary goal of liver perfusion imaging. Earlier detection of primary and metastatic hepatic malignancies and cirrhosis may be possible on the basis of relative increases in hepatic arterial blood flow associated with these diseases. To date, liver flow scintigraphy and flow quantification at Doppler ultrasonography have focused on characterization of global abnormalities. Computed tomography (CT) and magnetic resonance (MR) imaging can provide regional and global parameters, a critical goal for tumor surveillance. Several challenges remain: reduced radiation doses associated with CT perfusion imaging, improved spatial and temporal resolution at MR imaging, accurate quantification of tissue contrast material at MR imaging, and validation of parameters obtained from fitting enhancement curves to biokinetic models, applicable to all perfusion methods. Continued progress in this new field of liver imaging may have profound implications for large patient groups at risk for liver disease.

Intraoperative direct measurement of hepatic arterial buffer response in patients with or without cirrhosis

The hepatic arterial buffer response (HABR) is an intrinsic regulatory mechanism of the hepatic artery (HA) that compensates for reductions in portal venous (PV) blood flow. Whether this response is maintained in patients with cirrhosis (LC) is unclear. The aim of the present study was to examine whether HABR is maintained in patients with LC using direct blood flow measurements. PV and HA blood flow were intraoperatively measured and compared in patients with (LC group, n = 39) or without (control group, n = 22) cirrhosis at baseline (baseline HABR) and after PV clamping (acute HABR) using an ultrasound transit-time flowmeter. In contrast to the proportional relationship between the baseline PV and HA blood flow observed in the control group, HA blood flow and the HA-PV flow ratio increased when PV blood flow decreased in the LC group, suggesting that the baseline HABR had already been activated. Acute HABR, evaluated by the absolute and relative changes in HA blood flow and by the buffer capacity, was blunted in the LC group (P < 0.001, P < 0.01, and P = 0.01, respectively). An association between the degree of acute HABR impairment and the level of baseline HABR activation (HA-PV flow ratio) could not be confirmed in the LC group. In conclusion, the baseline HABR appears to be continuously activated in patients with LC; this phenomenon probably results in the impairment of the acute HABR.