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Portal Venous (portal + venous)

Distribution by Scientific Domains
Medical Sciences83%

Terms modified by Portal Venous

  • portal venous blood flow
    		•
  • portal venous flow
    		•
  • portal venous gas
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    Selected Abstracts

    Evaluation of Quantitative Portal Venous, Hepatic Arterial, and Total Hepatic Tissue Blood Flow Using Xenon CT in Alcoholic Liver Cirrhosis,Comparison With Liver Cirrhosis Related to Hepatitis C Virus and Nonalcoholic Steatohepatitis

    ALCOHOLISM, Issue 2010
    Hideaki Takahashi
    Background/Aims:, Xenon computed tomography (Xe-CT) is a noninvasive method of quantifying and visualizing tissue blood flow (TBF). For the liver, Xe-CT allows separate measurement of hepatic arterial and portal venous TBF. The present study evaluated the usefulness of Xe-CT as a noninvasive diagnostic procedure for measuring hepatic TBF in alcoholic liver cirrhosis (AL-LC), compared with liver cirrhosis related to nonalcoholic steatohepatitis (NASH), (NASH-LC), and hepatitis C virus (HCV), (C-LC). Methods:, Xe-CT was performed on 22 patients with AL-LC, 7 patients with NASH-LC, and 24 patients with C-LC. Severity of LC was classified according to Child-Pugh classification. Correlations between hepatic TBF, Child-Pugh classification, and indocyanin green retention (ICG) rate after 15 minutes (ICG15R) were examined. Correlations of hepatic TBF in Child-Pugh class A to AL-LC, NASH-LC, and C-LC were also examined. Results:, Portal venous TBF (PVTBF) displayed a significant negative correlation with Child-Pugh score and ICG15R (r = ,0.432, p < 0.01, r = ,0.442, p < 0.01, respectively). Moreover, ICG15R displayed a significant positive correlation with Child-Pugh score (r = 0.661, p < 0.001). Meanwhile, mean PVTBF and total hepatic TBF (THTBF) was significantly lower in AL-LC than in C-LC (p < 0.05). Mean PVTBF was significantly lower in Child-Pugh class A to AL-LC and NASH-LC than in that to C-LC (p < 0.05). Similarly, mean THTBF was significantly lower in Child-Pugh class A to NASH-LC than in that to C-LC (p < 0.05). Conclusions:, Measurement of hepatic TBF using Xe-CT is useful as a noninvasive, objective method of assessing the state of the liver in chronic liver disease. [source]

    MR-based visualization and quantification of three-dimensional flow characteristics in the portal venous system

    JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2010
    Zoran Stankovic MD
    Abstract Purpose: To evaluate the feasibility of time-resolved flow-sensitive MRI for the three-dimensional (3D) visualization and quantification of normal and pathological portal venous (PV) hemodynamics. Materials and Methods: Portal venous hemodynamics were evaluated in 18 healthy volunteers and 5 patients with liver cirrhosis. ECG- and adaptive respiratory navigator gated flow-sensitive 4D MRI (time-resolved 3D MRI with three-directional velocity encoding) was performed on a 3 Tesla MR system (TRIO, Siemens, Germany). Qualitative flow analysis was achieved using 3D streamlines and time-resolved particle traces originating from seven emitter planes precisely placed at anatomical landmarks in the PV system. Quantitative analysis included retrospective extraction of regional peak and mean velocities and vessel area. Results were compared with standard 2D flow-sensitive MRI and to the reference standard Doppler ultrasound. Results: Qualitative flow analysis was successfully used in the entire PV system. Venous hemodynamics in all major branches in 17 of 18 volunteers and 3 of 5 patients were reliably depicted with good interobserver agreement (kappa = 0.62). Quantitative analysis revealed no significant differences and moderate agreement for peak velocities between 3D MR and 2D MRI (r = 0.46) and Doppler ultrasound (US) (r = 0.35) and for mean velocities between 3D and 2D MRI (r = 0.41). The PV area was significantly (P < 0.01) higher in 3D and 2D MRI compared with US. Conclusion: We successfully applied 3D MR velocity mapping in the PV system, providing a detailed qualitative and quantitative analysis of normal and pathological hemodynamics. J. Magn. Reson. Imaging 2010;32:466,475. © 2010 Wiley-Liss, Inc. [source]

    Morphological mechanisms for regulating blood flow through hepatic sinusoids

    LIVER INTERNATIONAL, Issue 1 2000
    Robert S. McCuskey
    Abstract: This review summarizes what is known about the various morphological sites that regulate the distribution of blood flow to and from the sinusoids in the hepatic microvascular system. These sites potentially include the various segments of the afferent portal venules and hepatic arterioles, the sinusoids themselves, and central and hepatic venules. Given the paucity of smooth muscle in the walls of these vessels, various sinusoidal lining cells have been suggested to play a role in regulating the diameters of sinusoids and influencing the distribution and velocity of blood flow in these vessels. While sinusoidal endothelial cells have been demonstrated to be contractile and to exhibit sphincter function, attention has recently focused on the perisinusoidal stellate cell as the cell responsible for controlling the sinusoidal diameter. A very recent study, however, suggested that the principal site of vasoconstriction elicited by ET-1 was the pre-terminal portal venule. This raised the question of whether or not the diameters of sinusoids might decrease due to passive recoil when inflow is reduced or eliminated and intra-sinusoidal pressure falls. In more recent in vivo microscopic studies, clamping of the portal vein dramatically reduced sinusoidal blood flow as well as the diameters of sinusoids. The sinusoidal lumens rapidly returned to their initial diameters upon restoration of portal blood flow suggesting that sinusoidal blood pressure normally distends the sinusoidal wall which can recoil when the pressure drops. Stellate cells may be responsible for this reaction given the nature of their attachment to parenchymal cells by obliquely oriented microprojections from the lateral edges of their subendothelial processes. This suggests that care must be exercised when interpreting the mechanism for the reduction of sinusoidal diameters following drug administration without knowledge of changes occurring to the portal venous and hepatic inflow. [source]

    Transhepatic lactate gradient in relation to liver ischemia/reperfusion injury during major hepatectomies

    LIVER TRANSPLANTATION, Issue 12 2006
    Kassiani Theodoraki
    Hepatectomies performed under selective hepatic vascular exclusion are associated with a series of events culminating in ischemia/reperfusion injury, a state that shares common characteristics with situations known to result in global or regional hyperlactatemia. Accordingly, we sought to determine whether lactate is released by the liver during hepatic resections performed under blood flow deprivation and what relation this has to a possible systemic hyperlactatemic state. After ethical approval, 14 consecutive patients with resectable liver tumors subjected to hepatectomy under inflow and outflow occlusion of the liver were studied. Lactate concentrations were assessed in simultaneously drawn arterial, portal venous, and hepatic venous blood before liver dissection and 50 minutes postreperfusion. Moreover, the transhepatic lactate gradient (hepatic vein , portal vein) was calculated to see if there was net production or consumption of lactate. Before hepatic dissection, the transhepatic lactate gradient was negative, suggesting consumption by the liver. Fifty minutes after reperfusion, this gradient became significantly positive, demonstrating release of lactate by the liver (0.12 ± 0.31 vs. ,0.38 ± 0.30 mmol/L, P < 0.05). The magnitude of lactate release correlated with systemic arterial lactate levels at the same time point (r2 = 0.63, P < 0.001). A weaker but significant correlation was demonstrated between the transhepatic lactate gradient postreperfusion and systemic arterial lactate levels 24 hours postoperatively (r2 = 0.41, P = 0.013). A strong correlation between the transhepatic lactate gradient postreperfusion and peak postoperative aspartate aminotransferase values was also demonstrated (r2 = 0.73, P < 0.001). The liver becomes a net producer of lactate in hepatectomies performed under blood flow deprivation. This lactate release can explain some of the systemic hyperlactatemia seen in this context and relates to the extent of ischemia/reperfusion injury. Liver Transpl 12:1825-1831, 2006. © 2006 AASLD. [source]

    Intestinal and hepatic metabolism of glutamine and citrulline in humans

    THE JOURNAL OF PHYSIOLOGY, Issue 2 2007
    Marcel C. G. Van De Poll
    Glutamine plays an important role in nitrogen homeostasis and intestinal substrate supply. It has been suggested that glutamine is a precursor for arginine through an intestinal,renal pathway involving inter-organ transport of citrulline. The importance of intestinal glutamine metabolism for endogenous arginine synthesis in humans, however, has remained unaddressed. The aim of this study was to investigate the intestinal conversion of glutamine to citrulline and the effect of the liver on splanchnic citrulline metabolism in humans. Eight patients undergoing upper gastrointestinal surgery received a primed continuous intravenous infusion of [2- 15N]glutamine and [ureido- 13C,2H2]citrulline. Arterial, portal venous and hepatic venous blood were sampled and portal and hepatic blood flows were measured. Organ specific amino acid uptake (disposal), production and net balance, as well as whole body rates of plasma appearance were calculated according to established methods. The intestines consumed glutamine at a rate that was dependent on glutamine supply. Approximately 13% of glutamine taken up by the intestines was converted to citrulline. Quantitatively glutamine was the only important precursor for intestinal citrulline release. Both glutamine and citrulline were consumed and produced by the liver, but net hepatic flux of both amino acids was not significantly different from zero. Plasma glutamine was the precursor of 80% of plasma citrulline and plasma citrulline in turn was the precursor of 10% of plasma arginine. In conclusion, glutamine is an important precursor for the synthesis of arginine after intestinal conversion to citrulline in humans. [source]

    Portal Venous Donor-Specific Transfusion in Conjunction with Sirolimus Prolongs Renal Allograft Survival in Nonhuman Primates

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009
    K. K. Dhanireddy
    Pretransplant exposure to donor antigen is known to modulate recipient alloimmunity, and frequently results in sensitization. However, donor-specific transfusion (DST) can have a protolerant effect that is dependent on route, dose and coadministered immunosuppression. Rodent studies have shown in some strain combinations that portal venous (PV) DST alone can induce tolerance, and uncontrolled clinical use of PVDST has been reported. In order to determine if pretransplant PVDST has a clinically relevant salutary effect, we studied it and the influence of concomitant immunosuppression in rhesus monkeys undergoing renal allotransplantation. Animals received PVDST with unfractionated bone marrow and/or tacrolimus or sirolimus 1 week prior to transplantation. Graft survival was assessed without any posttransplant immunosuppression. PVDST alone or in combination with tacrolimus was ineffective. However, PVDST in combination with sirolimus significantly prolonged renal allograft survival to a mean of 24 days. Preoperative sirolimus alone had no effect, and peripheral DST with sirolimus prolonged graft survival in 2/4 animals, but resulted in accelerated rejection in 2/4 animals. These data demonstrate that PVDST in combination with sirolimus delays rejection in a modest but measurable way in a rigorous model. It may thus be a preferable method for donor antigen administration. [source]