Portal Vein Hemodynamics Research Articles

Doppler ultrasound in prediction of the early mortality risk factors on the waiting list for pediatric liver transplantation recipients

UE TO SHORTAGE of organ donation, limited manpower, and financial resources, a high mortality rate was found on the waiting list for pediatric liver transplantation. The purpose of this study was to document the variable changes in the hemodynamics of hepatic artery and portal vein by Doppler ultrasound and to assess their significance to the mortality in the waiting list and the need for early surgical intervention of liver transplantation for life-saving purposes. MATERIALS AND METHODS There were 36 pediatric patients included in this study (17 girls and 19 boys, age from 0.5 to 7.8 years old, mean age of 1.8 years) with underlying diseases of biliary atresia (29), glycogen storage disease (3), idiopathic portal hypertension (2), type I choledochal cyst (1), and liver hemangioendothelioma (1). We carried out monthly Doppler sonography examination on these potential recipients waiting for a liver transplant for the past 2 years to obtain progressive update data. Ultrasound examinations were performed by a single observer experienced in abdominal and Doppler techniques, using an Acuson 128XP10 (Acuson, Mountain View, Calif, USA) machine with a 3.5- to 7.0-MHz transducer available for color Doppler imaging. All the measurements of the portal veins were obtained at the extrahepatic portion of the main portal vein near the bifurcation. The portal flow direction was recorded as hepatopetal or hepatofugal. The angle-corrected flow velocity and cross-sectional area of the portal vein were obtained at the same site. The sample volume size for the Doppler scan was set at 1 to 3 mm, about half the diameter of the measured portal vein. This velocity was corrected by the angle (within 30 to 60 degrees) between the long axis of the portal vein and the Doppler beam. We calculated the portal flow volume per body weight as described by Kawasaki et al 1 The portal blood flow volume (PBFV) was calculated using the formula: PBFV 5 portal vein time average velocity (TAV) (cm/ s) 3 portal vein cross sectional area (A) (cm 2 ) 3 60/body weight (BW) (kg). Measurements of the hepatic artery including Doppler US waveform, peak systolic velocity (PSV), and resistance index (RI) were obtained along the hepatic hilum. The PSV of the hepatic artery was detected and corrected along the long axis of the color-coded hepatic artery. The angle between the long axis of the color-coded vessel and the Doppler beam was less than 30 degrees. The Doppler sample volume was set about 1 to 2 mm as half to the measured arterial caliber. The pulse repetition frequency was maintained at the lowest possible shift range to avoid aliasing. An average of three tracing of all the measurements obtained at the same site were used to generate a mean PSV and RI. The hepatic artery resistance index (HARI) was calculated automatically by the computer software of the ultrasound machine by the formula: HARI 5 (S 2 D)/S, where S is peak systolic velocity and D is end diastolic velocity. We divided the studied cases into two groups respectively by each of variable factors such as age, body weight, fever (septicemia), esophageal varices (E-V) bleeding, severe jaundice, amount of ascites, PBFV, and HARI, which may be significant as high risk factors of mortality. RESULTS Of the 36 children waiting for liver transplantation, all underwent Doppler ultrasound examination of preoperative evaluation for hepatic hemodynamics in the past 1 year. There were six cases of mortality in the 36 cases studied, and overall cumulative mortality rate in the past 1 year was 18%. There were 10 cases that received liver transplantation for life-saving reasons in subsequent time, and they were all alive; these cases were excluded for survival analysis, thus the mortality of the waiting list should be corrected. Therefore the mortality rate was 23% higher on these 26 cases of nontransplantation. ANALYSIS OF THE PREDICTIVE RISK FACTORS

7107 Clinical significance of hepatocyte growth factor and portal blood flow as a parameter of hepatic function following cO2pneumoperitoneum in cirrhotic patients.

Background: Laparoscopic surgery under carbon dioxide (CO2) pneumoperitoneum has many benefits. However, little is known concerning the risks of CO2pneumoperitoneum for the patients with liver cirrhosis. Influence of CO2pneumoperitoneum for the cirrhotic patients was investigated by assessing hemodynamics of portal vein and change of cytokine. Material & Methods: Participants were cholelithiasis patients divided into two groups: Group I (with liver cirrhosis: LC, n=12), and Group II (without liver cirrhosis: Control, n=12). The cross section area of the portal vein trunk (S) and the velocity of the portal blood (V) were measured using a laparoscopic pulsed Doppler ultrasonic probe (Aloka Ind., Ltd., Tokyo, Japan) inserted through the epigastric trocar when the abdomen was insufflated to an intra-abdominal pressure (IAP) of 4mmHg to 15 mm Hg preoperatively. The mean portal blood flow Φ at each IAP was calculated from the measured variables of S and V. In addition, plasma level of hepatocyte growth factor (HGF), interleukin (IL)-6, IL-8, tumor necrosis factor (TNF) were measured during CO2pneumopeitoneum. Total bilirubin (Tbil), AST, ALT were measured at postoperative day 1(1POD). Results: Laparoscopic cholecystectomy was performed successfully without any complications in all cases. With increases in IAP, S and V value were significantly decreased only in the LC group. F value was also significantly decreased with elevation of IAP in the LC group. No significant differences in changes of IL-6, IL-8 and TNF value during the preoperative CO2pneumopeitoneum were found in both group, but only HGF showed significant differences in changes of IAP in LC group. HGF and F value in IAP of 15mmHg showed significant correlations with AST and ALT at 1POD. Conclusions: On the basis of these results, HGF and F value were considered to be a good indicator for evaluation of liver function and CO2pneumopeitoneum during laparoscopic surgery would be a deteriorating factor for the patients with liver cirrhosis.

Portal vein and superior mesenteric artery hemodynamics in cirrhotic patients with gastroesophageal varices

Portal vein and superior mesenteric artery hemodynamics in cirrhotic patients with gastroesophageal varices

Portal vein hemodynamics in cirrhotic patients with portal hypertensive gastropathy: An echo doppler study

Background & Aims: Hydrogen sulfide (H2S), an endogenous gaseous mediator that causes vasodilation, is generated in mammalian tissues by cystathionine β-synthase (CBS) and cystathionine-γ-lyase (CSE). Here, we have investigated the role of H2S in a rodent model of nonsteroidal anti-inflammatory drug (NSAID) gastropathy. Methods: Rats were given acetyl salycilic acid (ASA) or an NSAID alone or in combination with NaHS, an H2S donor, and killed 3 hours later. Gastric blood flow was measured by laser-Doppler flowmetry, whereas intravital microscopy was used to quantify adhesion of leukocytes to mesenteric postcapillary endothelium. Results: At a dose of 100 μmol/kg, NaHS attenuated by 60%–70% the gastric mucosal injury, and tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, and lymphocyte function-associated antigen (LFA)-1 mRNA up-regulation induced by NSAIDs (P < .05) NaHS administration prevented the associated reduction of gastric mucosal blood flow (P < .05) and reduced ASA-induced leukocyte adherence in mesenteric venules. NaHS did not affect suppression of prostaglandin E2 (PGE2) synthesis by NSAIDs. Glibenclamide, a KATP channel inhibitor, and DL-propargylglycine, a CSE inhibitor, exacerbated, whereas pinacidil, a KATP opener, attenuated gastric injury caused by ASA. Exposure to NSAIDs reduced H2S formation and CSE expression (mRNA and protein) and activity by 60%–70%. By promoter deletion and mutation analysis, an Sp1 consensus site was identified in the CSE promoter. Exposure to NSAIDs inhibits Sp1 binding to its promoter and abrogates CSE expression in HEK-293 cells transfected with a vector containing the core CSE promoter. Exposure to NSAIDs inhibits Sp1 and ERK phosphorylation. Conclusions: These data establish a physiologic role for H2S in regulating the gastric microcirculation and identify CSE as a novel target for ASA/NSAIDs.

Portal Vein Hemodynamics in Patients with Biliary Atresia

Portal Vein Hemodynamics in Patients with Biliary Atresia

Effect of propranolol on portal vein hemodynamics: assessment by duplex sonography and indocyanine green clearance in healthy volunteers

In the past decade several randomized trials have shown a beneficial effect of propranolol in cirrhotic patients. The effect of propranolol has been attributed to a reduction in portal vein pressure. So far the monitoring of portal vein hemodynamics following propranolol administration has been achieved mainly by hepatic vein catheterization. We studied the effect of propranolol on portal vein hemodynamics noninvasively in five healthy volunteers using duplex sonography and indocyanine green clearance. Measured by duplex sonography, blood flow was reduced by 28.6% in the portal vein (P < 0.05) and by 8.7% in the hepatic artery (NS) 60 min after oral administration of 80 mg propranolol. During this time total hepatic blood flow, measured by indocyanine green clearance, was reduced by 19.5% (P < 0.05). We conclude that both methods are useful for the study of portal vein hemodynamics during propranolol therapy, duplex sonography being more easily practicable.

Changes in portal vein hemodynamics after hepatic portoenterostomy : K. Tanaka, I. Shirabase, S. Uemoto, et al. Pediatr Surg Int 7:260–264, (June), 1992

Changes in portal vein hemodynamics after hepatic portoenterostomy : K. Tanaka, I. Shirabase, S. Uemoto, et al. Pediatr Surg Int 7:260–264, (June), 1992

Changes in portal vein hemodynamics after hepatic portoenterostomy in biliary atresia

Portal vein (PV) shrinkage sometimes eliminates the possibility of liver transplantation in biliary atresia patients after hepatic portoenterostomy. To determine the factors leading to PV shrinkage, we performed a serial sonographic study of the portal venous system in 21 children. Cross-sectional PV area and mean portal venous velocity (PVV) were reduced in patients with refractory cholangitis and those with gastroesophageal varices and cholangitis. Although the reduction in cross-sectional PV area was greater in patients with four-time laparotomy than single laparotomy, the mean PVV was not reduced by repeated laparotomy. Patients with varices were lower in age, weight, mean PVV, cross-sectional PV area for age, and had higher serum total bilirubin levels. In conclusion, refractory cholangitis is a significant factor in shrinking the PV. With active bile drainage, varices spontaneously regress, the PV increases in both caliber and total length per unit hepatic volume, and PVV normalizes. It is suggested that pulsed Doppler PV sonography can help to determine the optimal time for liver transplantation referral in biliary atresia patients with progressive cirrhosis.

Hemodynamics of intrahepatic portal vein studied in healthy subjects and liver cirrhosis by pulsed Doppler method

Hemodynamics of intrahepatic portal vein studied in healthy subjects and liver cirrhosis by pulsed Doppler method

Evaluation of postprandial hyperemia in superior mesenteric artery and portal vein in healthy and cirrhotic humans: An operator-blind echo-Doppler study

In an operator-blind design, we used an echo-Doppler duplex system to examine superior mesenteric artery and portal vein hemodynamics on two consecutive mornings in 12 fasting cirrhotic patients and 12 matched controls, randomized to a standardized 355 kcal mixed-liquid meal vs. water. Cross-sectional area and mean velocity were recorded from the portal vein and superior mesenteric artery at 30 min intervals, from 0 min to 150 min after ingestion. Flows were calculated. Pulsatility index, an index related to vascular resistance, was obtained for the mesenteric artery. Baseline flows did not differ between cirrhotic patients and control patients, but pulsatility index was reduced in the cirrhotic subjects. Maximal postprandial hyperemia was attained at 30 min. Cirrhotic patients showed a blunted hyperemic response to food. In normal controls, portal vein area increased significantly after the meal from 30 min to 150 min, whereas in cirrhotic patients a significant difference occurred only at 30 min. Pulsatility index in both groups was significantly reduced after eating, and this reduction persisted up to 150 min. No changes after ingestion of water were observed. Echo-Doppler was very sensitive in detecting postprandial splanchnic hemodynamic changes and differences between cirrhotic patients and normal subjects. Mesenteric artery pulsatility index was more sensitive than flow in detecting baseline hemodynamic differences. In cirrhotic patients, portal postprandial hyperemia was mainly related to the increase in mean velocity.

Effect of Metoclopramide on Portal Blood Flow in Patients with Liver Cirrhosis, Measured by the Pulsed Doppler System

The effect of metoclopramide on portal blood flow, the maximal diameter of the portal vein, and some cardiovascular haemodynamic variables was studied in 10 patients with cirrhosis of the liver and portal hypertension. Portal vein haemodynamics were studied by the pulsed Doppler system. Within 15 min of intravenous administration of 20 mg metoclopramide, portal blood velocity and portal blood flow decreased significantly, from 11.2 +/- 1.1 to 10.8 +/- 1.2 cm/sec and from 769.0 +/- 87.7 to 707.9 +/- 84.2 ml/min, respectively (p less than 0.001). Within about 30 min portal blood velocity and portal blood flow returned to basal values (p greater than 0.05). The maximal diameter of the portal vein, systolic and diastolic blood pressure, and heart rate remained unchanged. These results support the hypothesis that metoclopramide, which raises lower oesophageal sphincter pressure and reduces intravariceal blood flow, significantly decreases the portal blood flow in cirrhotic patients with portal hypertension.

Influence of the Degree of Liver Failure on Portal Blood Flow in Patients with Liver Cirrhosis

Portal vein haemodynamics as demonstrated by the pulsed Doppler system were studied in 37 patients with cirrhosis who had been classified in three groups (A, B, and C) in accordance with the degree of liver failure. Maximal inner diameter of the portal vein was significantly lower in patients who were considered to be in good condition (group A) than in patients with moderate and severe liver failure (group B and group C) (p less than 0.001). A significant difference was also found between group A and group B and between group A and group C with regard to the portal blood velocity and portal blood flow (p less than 0.001). In accordance with the presence and size of the oesophageal varices, in patients with large varices the portal blood velocity and portal blood flow were significantly lower than in patients without varices (p less than 0.001), whereas maximal inner portal vein diameter was significantly higher (p less than 0.001). This study demonstrated that in patients with cirrhosis circulatory alterations in the portal vascular bed may be, at least in part, an indicator of the stage of liver disease.

Continuous monitoring of portal vein and hepatic artery hemodynamics in unrestrained rats.

Continuous measurement of portal vein and hepatic artery blood flows during physiological experimental conditions, even in large animals, poses difficult problems. We report the successful use of miniaturized flow probes and pulsed Doppler flowmetry for chronic monitoring of hepatic artery and portal vein flows in intact unrestrained rats and describe the probe construction and implantation. Proportionality between portal vein velocity and portal flow was made possible by a technique for stabilizing the diameter of the venous segment from which velocity is recorded. The accuracy of the method in detecting changes in portal vein flow was established by the high statistically significant correlation between changes in velocity recorded simultaneously from portal vein and superior mesenteric artery in a series of rats with ligated celiac and inferior mesenteric arteries. In these preparations all portal vein flow is derived from the superior mesenteric artery. Complex dynamic changes in the hepatic circulation of conscious unrestrained rats were recorded in response to systemic injections of glucagon and angiotensin II. In the resting state several characteristic velocity patterns were recorded from the portal vein. Oscillations linked to respiration were not observed while the animals rested quietly but were noted during sleep and anesthesia. Two hitherto unrecognized patterns produced respectively by the pulsations of the superior mesenteric artery and by spontaneous contractions of the portal vein were also observed. The method described here provides the first opportunity to study hepatic circulation in chronically instrumented rats during physiological experimental conditions.

Portal vein hemodynamics in response to acute B-blocker and vasodilatatory treatment in liver cirrhosis

Portal vein hemodynamics in response to acute B-blocker and vasodilatatory treatment in liver cirrhosis