Portal Venous Flow Research Articles

Hepatic encephalopathy as a complication of liver cirrhosis: An Asian perspective

Hepatic encephalopathy is one of the most important clinical manifestations in decompensated liver cirrhosis. Accepted concepts regarding the pathophysiology of hepatic encephalopathy are that the endogenous neurotoxic substances, including ammonia: (i) escape from catabolism by the liver due both to the impaired function of the cirrhotic liver and also to the presence of portal systemic shunting; (ii) circulate at elevated concentrations in the systemic blood flow; (iii) reach the brain through the blood-brain barrier; and (iv) impair cerebral function leading to disturbances of consciousness. The majority of these toxic substances are produced in the intestine by the bacterial flora, and are absorbed into the portal venous flow. The epidemiology of liver cirrhosis depends particularly on its etiology, and shows a marked geographic difference worldwide between Western, and Asian countries. Hepatic encephalopathy developed at an annual rate of 8% in cirrhotics in Far Eastern studies. In Eastern and Far East countries, therapeutic options are similar to those in the western hemisphere, but pronounced application of dietary restriction, antimicrobial agents, disaccharides, shunt obliteration and branched chain amino acids is noted. In spite of improved therapeutic options for encephalopathy, the long-term survival is still low. Thus, hepatic encephalopathy remains a serious complication of liver cirrhosis. Establishment of truly effective prevention modalities and broader application of liver transplantation will help rescue patients suffering from this complication of liver cirrhosis in the near future.

Risk factors for portal venous thrombosis after splenectomy in patients with cirrhosis and portal hypertension

Portal venous thrombosis (PVT) is a potentially fatal complication following splenectomy. Its mechanisms and risk factors are poorly understood, especially in patients with cirrhosis and portal hypertension. This study investigated risk factors for PVT following splenectomy in such patients. All consecutive patients with cirrhosis who underwent splenectomy in Kyushu University Hospital between 1998 and 2004 were included in this retrospective study. They were divided into two groups based on the presence or absence of postoperative PVT. Preoperative and operative factors were compared, and the relationships between formation of PVT and its independent variables were analysed. In some cases, portal venous flow was measured before and after splenectomy using duplex Doppler ultrasonography. PVT developed after surgery in 17 (24 per cent) of 70 patients studied. Multivariable analysis showed that increased splenic vein diameter and low white cell count were significant independent risk factors for PVT. Portal venous flow after splenectomy was greatly reduced in the PVT group, but not in patients without PVT. Large splenic vein diameter and low white cell count are independent risk factors for PVT after splenectomy in patients with cirrhosis and portal hypertension.

Effect Of PPADS On Mesenteric Arterial And Portal Venous Flow Responses To Splanchnic Nerve Stimulation

Our previous work suggested that splanchnic nerve stimulation may exert differential effects on mesenteric arterial and portal venous hemodynamics. This study tested the hypothesis that ATP contributes to the differences in mesenteric arterial and portal venous responses to splanchnic nerve stimulation.Spontaneously hypertensive rats (SHR) were anesthetized with urethane/chloralose and fitted with catheters to record arterial pressure. The rats were also instrumented for splanchnic nerve stimulation and for mesenteric arterial and portal venous blood flow recording. Frequency response curves (1–15 Hz) were constructed before and after treatment with pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulfonate (PPADS; 20 mg/kg), an ATP P2X receptor antagonist.Splanchnic nerve stimulation caused frequency dependent decreases in mesenteric arterial and portal venous blood flow. Treatment with PPADS caused a rightward displacement of the frequency response curves for both mesenteric arterial flow and portal venous flow. The magnitude of this displacement was less than that observed following omega conotoxin treatment.Collectively, these data suggest that ATP contributes to both mesenteric arterial and portal venous responses to splanchnic nerve stimulation. Supported by NIH #2RO1HL63053‐ARRA (DM) and USD SSOM bridge funds.

Computer-Based Liver Volumetry in the Liver Perfusion Simulator

An exact preoperative liver volume calculation is important prior to liver surgery and living-related liver transplantation. However, CT or MRI assessment of preoperative liver volume is associated with an estimation error of 1.2% to 36%, and little data is available on its accuracy on the segmental level. The aim of this study was to validate arterial and portal venous flow rates and gain information on liver volumetry, including liver segments, in the liver perfusion simulator and compare it to in vivo measurements in a porcine model. The arterial and portal venous flow rates and liver volumes of 10 pigs were measured in vivo and compared with the flow rates and volumes ex vivo. CT scans were performed and the volume of the liver and its lobes calculated by water displacement or computer-assistance based on the CT scans. The right lateral lobe was plasticized and reconstructed for the volume calculation. In the liver perfusion simulator, arterial and portal venous flow rates comparable to the in vivo rates were achieved. The liver volume had a mean difference of 10.3% between in vivo and ex vivo measurements. In the liver perfusion simulator, the mean deviation in liver volume between the computer calculation and water displacement was 2.8%. On the segmental level, the Heidelberg algorithm provided an accuracy of 97.7%. The liver perfusion simulator is an excellent device for studies in liver perfusion and volumetry. Furthermore, the simulator is applicable for teaching and performing interventions and surgeries in livers.

Portal hyperperfusion: Mechanism of injury and stimulus for regeneration in porcine small-for-size transplantation

Understanding the pathogenesis of small-for-size (SFS) syndrome is critical to expanding the applicability of partial liver transplantation. We aimed to characterize its acute presentation and association with alterations in hepatic hemodynamics, microstructure, and regeneration in a porcine model. Eighteen SFS liver transplants were performed. Donors underwent 70% hepatectomy. Partial grafts were implanted into larger recipients. Whole liver transplants were also performed (n = 6). Recipients were followed until death or for 5 days. Hemodynamics were measured, and tissue was sampled intraoperatively and at the study end. Serum was sampled regularly during follow-up. Seventeen SFS transplants and 6 whole liver transplants were included. SFS grafts represented 23.2% (19.3%-25.3%) of the recipients' standard liver volume. The survival rate was 29% and 100% in the SFS and whole liver groups, respectively. The portal venous flow, pressure gradient, and resistance were significantly higher in recipients of SFS grafts versus whole livers after portal and arterial reperfusion. Arterial flow as a percentage of the total liver blood flow was significantly lower after reperfusion in SFS grafts and remained so when measured again after 5 days. Markers of endothelial cell injury increased soon after reperfusion, and those of hepatocellular injury increased later; both predicted the appearance of either graft failure or histological recovery. Proliferative activity peaked earlier and higher among nonsurvivors in the SFS group. Surviving grafts demonstrated a slower but maintained rise in regenerative activity, although metabolic activity failed to improve. In SFS transplantation in the acute setting, portal hyperperfusion is a stimulus for regeneration but may simultaneously cause irreparable endothelial injury. This porcine model not only helps to elucidate the inciting factors in SFS pathogenesis but also offers a clinically relevant means to study its prevention.

Diagnosis of cirrhosis with intravoxel incoherent motion diffusion MRI and dynamic contrast‐enhanced MRI alone and in combination: Preliminary experience

To report our preliminary experience with the use of intravoxel incoherent motion (IVIM) diffusion-weighted magnetic resonance imaging (DW-MRI) and dynamic contrast-enhanced (DCE)-MRI alone and in combination for the diagnosis of liver cirrhosis. Thirty subjects (16 with noncirrhotic liver, 14 with cirrhosis) were prospectively assessed with IVIM DW-MRI (n = 27) and DCE-MRI (n = 20). IVIM parameters included perfusion fraction (PF), pseudodiffusion coefficient (D*), true diffusion coefficient (D), and apparent diffusion coefficient (ADC). Model-free DCE-MR parameters included time to peak (TTP), upslope, and initial area under the curve at 60 seconds (IAUC60). A dual input single compartmental perfusion model yielded arterial flow (Fa), portal venous flow (Fp), arterial fraction (ART), mean transit time (MTT), and distribution volume (DV). The diagnostic performances for diagnosis of cirrhosis were evaluated for each modality alone and in combination using logistic regression and receiver operating characteristic analyses. IVIM and DCE-MR parameters were compared using a generalized estimating equations model. PF, D*, D, and ADC values were significantly lower in cirrhosis (P = 0.0056-0.0377), whereas TTP, DV, and MTT were significantly increased in cirrhosis (P = 0.0006-0.0154). There was no correlation between IVIM- and DCE-MRI parameters. The highest Az (areas under the curves) values were observed for ADC (0.808) and TTP-DV (0.952 for each). The combination of ADC with DV and TTP provided 84.6% sensitivity and 100% specificity for diagnosis of cirrhosis. The combination of DW-MRI and DCE-MRI provides an accurate diagnosis of cirrhosis.

Hemodynamic Effects of Combined Therapy Using Partial Splenic Embolization and Transjugular Retrograde Obliteration for Gastric Varices with Gastrorenal Shunt

The purpose of the present study was to investigate the short-term effects of combined therapy using partial splenic embolization (PSE) and transjugular retrograde obliteration (TJO) on the portal hemodynamics of gastric varices with a gastrorenal shunt. Sixteen patients with gastric varices and a gastrorenal shunt were included in this study. Partial splenic embolization was applied 2 weeks before TJO. The portal blood flow was measured by an ultrasonic duplex Doppler system, and the wedged hepatic venous pressure (WHVP) was measured by hepatic venous catheterization, before and after the combined therapy. The complete obliteration of the gastrorenal shunt and gastric varices was revealed by retrograde shuntography and computed tomography after TJO in all cases. The WHVP before and just after PSE was 23 +/- 7 and 19 +/- 7 mmHg, respectively, showing a significant change (P < 0.01). The WHVP before and the day after TJO was 20 +/- 5 mmHg and 22 +/- 6 mmHg, respectively, showing a significant change (P < 0.01). There was no significant difference between the WHVP before and after the combined therapy. The portal venous flow volume before and after the combined therapy were 514 +/- 146 and 512 +/- 161 ml/min, respectively, showing no significant change. However, the splenic venous flow volume before and after the combined therapy was 319 +/- 131 and 179 +/- 113 ml/min, respectively, showing a significant change (P < 0.05). The WHVP did not change after the combined therapy of PSE and TJO. Partial splenic embolization contributed to protecting portal congestion after TJO. We conclude that the combined therapy using PSE and TJO is an effective treatment for gastric varices from the portal hemodynamic point of view.

Portal Doppler ultrasound evaluation in myelitis by Schistosoma mansoni

The mechanism for development of schistosomal myelitis has not yet been completely understood. Few publications have tried to establish a link between the general clinical presentation of the illness and its neurological manifestations. To evaluated the portal blood flow in patients with schistosomal myelitis and controls. Forty-three individuals were evaluated using portal Doppler ultrasound. Group I consisted of 13 patients with the spinal form of schistosomiasis. Group II included 10 patients with intestinal and hepatointestinal forms of schistosomiasis, but no neurological symptoms; while group III involved 20 healthy controls. Portal venous speed and portal venous flow were significantly elevated in group I (p<0.001) compared with the others. Doppler ultrasound demonstrated a situation of high flow within the portal venous system of patients with schistosomal myelitis.

Abstract No. 111: Hepatocellular carcinoma tumor response after portal vein embolization

Abstract No. 111: Hepatocellular carcinoma tumor response after portal vein embolization

Hepatic effects of an open lung strategy and cardiac output restoration in an experimental lung injury

Ventilation with high positive end-expiratory pressure (PEEP) can lead to liver dysfunction. We hypothesized that an open lung concept (OLC) using high PEEP impairs liver function and integrity dependent on the stabilization of cardiac output. Juvenile female Pietrain pigs instrumented with flow probes around the common hepatic artery and portal vein, pulmonary and hepatic vein catheters underwent a lavage-induced lung injury. Ventilation was continued with a conventional approach (CON) using pre-defined combinations of PEEP and inspiratory oxygen fraction or with an OLC using PEEP set above the lower inflection point of the lung. Volume replacement with colloids was guided to maintain cardiac output in the CON(V+) and OLC(V+) groups or acceptable blood pressure and heart rate in the OLC(V-) group. Indocyanine green plasma disappearance rate (ICG-PDR), blood gases, liver-specific serum enzymes, bilirubin, hyaluronic acid and lactate were tested. Finally, liver tissue was examined for neutrophil accumulation, TUNEL staining, caspase-3 activity and heat shock protein 70 mRNA expression. Hepatic venous oxygen saturation was reduced to 18 + or - 16% in the OLC(V-) group, while portal venous blood flow decreased by 45%. ICG-PDR was not reduced and serum enzymes, bilirubin and lactate were not elevated. Liver cell apoptosis was negligible. Liver sinusoids in the OLC(V+) and OLC(V-) groups showed about two- and fourfold more granulocytes than the CON(V+) group. Heat shock protein 70 tended to be higher in the OLC(V-) group. Open lung ventilation elicited neutrophil infiltration, but no liver dysfunction even without the stabilization of cardiac output.

Extrahepatic Portal Venous Obstruction due to a Giant Hepatic Hemangioma Associated with Kasabach-Merritt Syndrome

We describe a patient with extrahepatic portal venous obstruction due to a giant hepatic hemangioma associated with Kasabach-Merritt syndrome. A 67-year-old woman presented with upper abdominal distension and appetite loss. The medical history was not relevant to the current disorder. Initial laboratory tests revealed the following: serum platelet count, 9.9 × 10⁴/µL; serum fibrinogen degradation products, 12 µg/mL; prothrombin time, 1.26; and serum fibrinogen, 111 mg/dL. Computed tomography demonstrated homogenous low-density areas, 15 cm in diameter, in the left lobe of the liver. Common hepatic arteriography revealed a hypervascular tumor with pooling of contrast medium in the delayed phase. The portal venous phase of supramesenteric arteriography revealed obstruction and cavernous transformation of the portal vein. We diagnosed extrahepatic portal venous obstruction due to a giant hepatic hemangioma associated with Kasabach-Merritt syndrome. Laparotomy was performed, and the liver was found to be markedly enlarged. After mobilization of the left lobe, left hepatectomy was performed with intermittent clamping. After resection, Doppler ultrasonography revealed recovery of the portal venous flow. The cavernous transformation shrank. Pathologic examination of the surgical specimen confirmed the presence of a giant benign hepatic cavernous hemangioma. The patient was discharged 16 days after operation. Laboratory data and complications improved after 2 months.

Hepatic Encephalopathy as a Complication of Liver Cirrhosis: An Asian Perspective

Hepatic encephalopathy is one of the most important clinical manifestations in decompensated liver cirrhosis. Accepted concepts regarding the pathophysiology of hepatic encephalopathy are that the endogenous neurotoxic substances, including ammonia: (i) escape from catabolism by the liver due both to the impaired function of the cirrhotic liver and also to the presence of portal systemic shunting; (ii) circulate at elevated concentrations in the systemic blood flow; (iii) reach the brain through the blood-brain barrier; and (iv) impair cerebral function leading to disturbances of consciousness. The majority of these toxic substances are produced in the intestine by the bacterial flora, and are absorbed into the portal venous flow. The epidemiology of liver cirrhosis depends particularly on its etiology, and shows a marked geographic difference worldwide between Western, and Asian countries. Hepatic encephalopathy developed at an annual rate of 8% in cirrhotics in Far Eastern studies. In Eastern and Far East countries, therapeutic options are similar to those in the western hemisphere, but pronounced application of dietary restriction, antimicrobial agents, disaccharides, shunt obliteration and branched chain amino acids is noted. In spite of improved therapeutic options for encephalopathy, the long-term survival is still low. Thus, hepatic encephalopathy remains a serious complication of liver cirrhosis. Establishment of truly effective prevention modalities and broader application of liver transplantation will help rescue patients suffering from this complication of liver cirrhosis in the near future.

Ligation of Left Renal Vein as a Salvage Procedure for Splenorenal Shunt After Living Donor Liver Transplantation: A Case Report

We describe a case of recovered portal flow by ligation of the left renal vein (LRV) as a salvage procedure for a spontaneous splenorenal shunt (SRS) occurring the next day after right liver living donor transplantation (LDLT). Doppler ultrasonography showed normal graft portal venous flow immediately after LDLT, but nearly total diversion of portal flow into the existing splenorenal shunt was observed on the next day. Portal flow normalized after ligation of the LRV by relaparotomy. The patient recovered fully without complication and was discharged on the 17th postoperative day. He remains well at 14 months after the operation, returning to his previous occupation. This case was neither associated with acute rejection nor with small-for-size graft, which may increase intrahepatic vascular resistance, causing portal flow steal through shunts. Even though patients with preoperative SRS show normal portal flow immediately after transplantation, close monitoring is necessary for a possible decrease or loss of portal flow. If portal flow becomes insufficient, ligation of LRV as a salvage procedure is an important option that can be considered even after transplantation.

Noninvasive functional liver blood flow measurement: comparison between bolus dose and steady-state clearance of sorbitol in a small-rodent model

Plasma clearance of D-sorbitol, a nontoxic polyol, occurs predominantly in the liver and has been used to measure functional liver blood flow after bolus and steady- state intravenous administration. However, it is not known which of these two administration methods is superior. Therefore, plasma D-sorbitol clearance was studied in an animal model both after a bolus dose and under steady-state (SS) conditions and compared directly with liver blood flow, under normal conditions, and after the induction of endotoxin (LPS) sepsis. Adult male Wistar rats (526 +/- 38 g body wt; n = 27) were anesthetized and mechanically ventilated. Hemodynamics, hepatic arterial flow, and portal venous flow were measured. Two groups were studied, namely healthy animals that served as controls and a sepsis group that received 5 mg/kg LPS intravenously (Escherichia coli O127:B8). Each animal received either a SS infusion (0.1 mg/100 g body wt per min) or a bolus (3 mg/100 g body wt) of a 5% D-sorbitol solution intravenously in a randomized order. After the initial measurements and a 60-min pause time in between (T(1/2,sorbitol) = 9 min), a crossover was done. The hepatic clearance of D-sorbitol in the control group showed a good correlation between bolus and SS (Spearman's r = 0.7681, P = 0.0004), and both techniques correlated well with total liver blood flow (TLBF) (r = 0.7239, P = 0.0023 and r = 0.7226, P = 0.0023, respectively). Also in the sepsis group there was a good correlation between bolus and SS sorbitol clearance (r = 0.6655, P = 0.0182). In the sepsis group, only the SS clearance correlated with TLBF (r = 0.6434, P = 0.024). In conclusion, in normal and under septic conditions, hepatic clearance of D-sorbitol either by bolus or a SS infusion is comparable. In healthy animals, this also correlated well with TLBF but not in septic conditions. However, this is expected because of the changes in the liver microcirculation, shunting, and decreased hepatocyte function in sepsis.

Targeting circulatory dysfunction in cirrhosis: Terlipressin and the hepatorenal syndrome

Hong Kong is adeveloped country with a relatively well-informed, highly literatesociety, so that levels of awareness regarding NAFLD are likely tobe much worse among less well-off populations with lower lit-eracy rates. This is worrying, given the magnitude of public healthproblems posed by NAFLD.NAFLD is one of the commonest, if not the commonest, liverdiseases in Western populations, affecting at least 24–42% ofadults.

Effects of terlipressin on systemic, hepatic and renal hemodynamics in patients with cirrhosis

Terlipressin has been shown to be effective in the management of hepatorenal syndrome. However, how terlipressin exerts its effect on the renal artery is unknown. The aim of the present study was to assess the effects of terlipressin on systemic, hepatic and renal hemodynamics in cirrhosis. Twenty-eight patients with cirrhosis and portal hypertension were studied. Systemic and hepatic hemodynamics, hepatic and renal arterial resistive indices and neurohumoral factors were measured prior to and 30 min after intravenous administration of 1 mg terlipressin (n = 19) or placebo (n = 9). After terlipressin, there were significant increases in both mean arterial pressure (P < 0.001) and systemic vascular resistance (P < 0.001), whereas heart rate (P < 0.001) and cardiac output (P < 0.001) decreased significantly. There was a significant decrease in the hepatic venous pressure gradient (P < 0.001). Portal venous blood flow also decreased significantly (P < 0.001). The mean hepatic arterial velocity increased significantly (P < 0.001). Although there was a significant decrease in the hepatic arterial resistive index (0.72 +/- 0.08 to 0.69 +/- 0.08, P < 0.001) and renal arterial resistive index (0.74 +/- 0.07 to 0.68 +/- 0.07, P < 0.001), portal vascular resistance was unchanged (P = 0.231). Plasma renin activity decreased significantly (P < 0.005), and there was a significant correlation between this decline and the decrease in renal arterial resistive index (r = 0.764, P < 0.005). The effects of terlipressin on systemic, hepatic and renal hemodynamics were observed similarly in patients with and without ascites. Placebo caused no significant effects. Terlipressin decreases hepatic and renal arterial resistance in patients with cirrhosis.

Transvenous Variceal Embolization during or after Living-donor Liver Transplantation to Improve Portal Venous Flow

Diversion of portal vein (PV) flow from the partial liver graft in living-donor liver transplantation (LDLT) can be life-threatening and warrant interruption of large collateral vessels. The purpose of this study is to evaluate the clinical efficacy of percutaneous or intraoperative transvenous embolization of portosystemic collateral vessels to improve PV inflow during or after LDLT. From 2000 to 2007, 105 of 1,435 patients (7%) who had undergone LDLT underwent percutaneous (n = 17) or intraoperative (n = 88) venography to evaluate the status of PV inflow and portosystemic collateral vessels. Among these 105 patients, 19 underwent percutaneous (n = 6) or intraoperative (n = 13) transvenous embolization of portosystemic collateral vessels to improve PV inflow. This included 12 men and seven women with a mean age of 46.5 years. Successful embolization of the portosystemic collateral vessels with subsequently improved PV inflow was achieved in all 13 patients (100%) treated with the intraoperative approach and in four of six (67%) patients treated with the percutaneous approach. During follow-up (median, 8 months), Doppler ultrasonography showed adequate PV inflow in 17 of 19 patients, and follow-up computed tomography showed that collateral flow to the varices disappeared in 13 patients and decreased in four patients. One patient died of acute reactivated hepatitis 2 months after the procedure. Overall clinical success was achieved in 16 of the 19 study patients (84%). Transvenous embolization of varices may be an effective method to improve PV inflow in LDLT recipients.

The retrospective analysis of surgical outcome of portal hypertension

To retrospectively analyze the surgical outcome of portal hypertension and explore the risk-factors of long-term survival after operation. The data of 149 patients (male 119, female 30, aged from 19 to 73 years old) with portal hypertension treated surgically from January 1996 to October 2007 was collected. Among these patients, there were 110 patients for Child A and 39 patients for Child B according to Child-Pugh classification. According to different surgical modality, all patients were divided into devascularization group (n = 85) and shunting group (n = 64). The follow-up rate was 78.8% and the average follow-up time was (46.3 +/- 30.4) months. The overall survival rates of 1-, 3-, 5- and 10-years were 95.6%, 88.7%, 83.4% and 65.1% respectively. Meanwhile the survival rates of 1-, 3-, 5- and 10-years in devascularization group and in shunting group were 95.4%, 87.7%, 80.6%, 56.3% and 95.8%, 90.1%, 86.8%, 72.6% respectively. There was no significant difference in survival rate between these two groups (P > 0.05). Child-Pugh classification has been the most important risk-factor that could influence long-term survival after operation by analysis of COX regression and it showed that the long-term survival time in Child A was longer than in Child B. The re-hemorrhage rates of 1-, 3- and 5-years in shunting group would be much better than in devascularization group. The rate of postoperative encephalopathy in devascularization group and shunting group was 6.9% and 6.1% respectively and there was no significant difference (P > 0.05). The portal venous pressure and flow of portal vein decreased significantly after shunting operation (P < 0.05). The mainly sole risk-factor of long-term survival for portal hypertension has been the classification of Child-Pugh, not surgical procedure. The individualized proximal splenorenal shunt is much better than devascularization in controlling variceal hemorrhage.

Non-alcoholic steatohepatitis induces non-fibrosis-related portal hypertension associated with splanchnic vasodilation and signs of a hyperdynamic circulationin vitroandin vivoin a rat model

Steatosis, without fibrosis, may lead to changes in liver blood flow, which are poorly understood, and to date have not been correlated to portal pressure and related haemodynamics. To study the temporal relation between progressive steatosis, portal pressure, systemic haemodynamics, vascular responsiveness, mesenteric and portal blood flow in methionine-choline-deficient diet (MCDD)-fed rats. Male Wistar rats fed the MCDD were examined at week (w) 0-1-2-3-4-5-6-7-8, respectively, including systemic haemodynamics and portal pressure. At w0-4-8, in vivo blood flow was measured in the portal vein and the superior mesenteric artery. Dose-response curves to phenylephrine (PE) were established in abdominal aortic rings. Histology showed 100% steatosis from w3 on. Fibrosis was absent. Significant inflammation was nearly absent upon w4. Portal pressure slightly increased at w2, reached a maximum at w4 [9.4 +/- 0.3 vs 2.9 +/- 0.6 mmHg at w0 (P=0.003)] and remained stable upon w8. Mean arterial blood pressure (MABP) decreased from w2 on [98.7 +/- 5.7 mmHg on w4 compared with 123.8 +/- 1.8 on w0 (P=0.002)]. Portal flow increased from 1.85 +/- 0.11 to 3.07 +/- 0.44 ml/min/100 g on w0 and w8 respectively (P=0.039). Mesenteric artery flow increased from 3.40 +/- 0.26 to 4.56 +/- 0.30 ml/min/100 g on w0 and w8 respectively (P=0.043). Vascular responsiveness to PE gradually decreased from 138 +/- 3% on w0 to 110 +/- 5% on w4 (P=0.013). Steatohepatitis induces significant portal hypertension (PHT) in the absence of fibrosis, associated with an increase in mesenteric arterial and portal venous flow, arterial hyporesponsiveness to vasoconstrictors and a decrease in MABP, indicating the presence of splanchnic vasodilation and hyperdynamic circulation. These alterations resemble those seen in cirrhotic PHT.

Redistribution pattern of fetal liver circulation in intrauterine growth restriction

OBJECTIVE. Fetal liver blood supply is an important determinant of fetal growth and adaptation. Most fetal liver blood supply is from the umbilical vein, but the portal vein contributes 14-20% and studies of low-risk pregnancies suggest the splanchnic arteries are also involved in the homeostasis of fetal liver perfusion. Here we determine the circulatory pattern of the fetal liver in intrauterine growth restriction (IUGR). DESIGN. Cross-sectional study. POPULATION. Thirty-one IUGR fetuses (estimated fetal weight <5th centile). METHODS. Pulsatility index (PI) measurements of the umbilical, middle cerebral, splenic, hepatic, and superior mesenteric arteries were compared with a reference population and related to umbilical venous flow, umbilico-caval pressure gradient (assessed by ductus venosus peak velocity) and venous distribution within the liver (assessed by flow velocity in the left portal vein). RESULTS. Thirteen of 31 IUGR fetuses had umbilical artery PI > 97.5 centile and 13 showed a middle cerebral artery brain-sparing pattern (PI Z-score < - 2). In IUGR, umbilical venous flow was lower and less umbilical blood was distributed to the right liver lobe, while the umbilico-caval pressure gradient was kept normal. The hepatic and splenic arteries, but not the superior mesenteric artery, had low PI compared with the reference population. CONCLUSIONS. IUGR fetuses with increased or normal umbilical artery PI maintained venous perfusion pressure to the liver while distributing less umbilical blood to the right liver lobe. They showed regional splanchnic arterial redistribution with low splenic and hepatic artery PI, implying increased portal venous flow and direct arterial contribution to hepatic perfusion, respectively.