Intrahepatic Blood Flow Research Articles

Association between a focal spared area in the fatty liver and intrahepatic efferent blood flow from the gallbladder wall: evaluation with color Doppler sonography.

The purpose of this study was to investigate whether fatty sparing adjacent to the gallbladder fossa is related to efferent blood flow from the gallbladder wall. Color and power Doppler sonography were performed in 80 patients with a fatty liver that appeared as a fine echogenic pattern with considerable deep attenuation on sonography. We analyzed whether color signal appeared around the spared area, the gallbladder wall, or both. Subsequently, when such signal was detected, pulse Doppler analysis of the signal was performed. Color signal indicating efferent blood flow from the gallbladder wall was detected in 25 (64%) of 39 patients with a focal spared area at the gallbladder fossa and in two (5%) of 41 patients without a focal spared area. This difference was statistically significant (p < .05). The waveform of efferent blood flow signals (n = 25) that were seen within spared areas was continuous in 23 (92%) of 25 patients and was pulsatile in the remaining two patients (8%). Blood flow from the gallbladder wall to areas of the spared liver was frequently revealed by color and power Doppler sonography; therefore, this blood flow may be associated with focal fatty sparing.

Involvement of intrasinusoidal hemostasis in the development of concanavalin A-induced hepatic injury in mice.

Concanavalin A (Con A) stimulation induces T-cell activation-associated hepatic injury. This study is designed to show the involvement of microcirculatory disturbance in the pathogenesis. Con A administration led to prominent intrasinusoidal hemostasis, which consisted of erythrocyte agglutination, lymphocyte/neutrophil sticking to endothelial cells, and platelet aggregation and degranulation, resulting in a marked decrease in the intrahepatic blood flow and elevation of portal perfusion pressure. After hemostasis, confluent hepatic necrosis occurred within the congested area of liver parenchyma. Reduction in the extent of hemostasis by the treatment with heparin (thrombin inhibitor) or cyproheptadine (serotonin inhibitor) decreased hepatic injury. Pretreatment with either anti-tumor necrosis factor alfa (TNF-alpha) or anti-interferon gamma (IFN-gamma) monoclonal antibody (MAb) moderately decreased hemostasis and hepatic injury, whereas combined use of two MAbs almost perfectly protected mice from these disorders. Complete obliteration of hemostasis and hepatic injury was also accomplished by the pretreatment with FK506 which suppressed TNF-alpha and IFN-gamma production. Intrasinusoidal accumulation of leukocytes and platelets was, however, not blocked by FK506, indicating that Con A activities other than the stimulation of cytokine production are responsible for this event. The administration of anti-CD3 MAb, a T-cell stimulant without agglutination activities, which elevated plasma cytokine levels in a comparable degree without inducing prominent leukocyte infiltration, did not induce hepatic congestion and injury. These findings indicate that the agglutination activities of Con A and T-cell activation mediated TNF-alpha/IFN-gamma production are both required for the induction of intrasinusoidal hemostasis, which is indispensable for the development of hepatic injury.

Intrahepatic blood flow distribution in the perfused rat liver: effect of hepatic artery perfusion.

Variations in blood flow to different sinusoids within the liver can prevent uniform uptake of solutes from plasma and contribute to cellular ischemia in low-flow states. However, the degree of variability and the role of hepatic artery perfusion in maintaining uniform flow are poorly defined. We used an indicator dilution technique to compare the distribution of sinusoidal transit times in isolated rat livers perfused through the portal vein alone with livers perfused using both portal vein and hepatic artery. Physiological flow rates were used in each case (1.2 +/- 0.3 ml.min-1.g liver-1), but the second group received 32% of flow through the hepatic artery. Intralobular flow heterogeneity was further assessed by gamma counting of small (approximately 100 mg) pieces of the liver after bolus injection of approximately 5 mCi of a highly extracted compound ([125I])triiodothyronine) into the portal vein. Hepatic artery perfusion had no significant effect on mean sinusoidal transit time or intrahepatic distribution volume for 51Cr-labeled red blood cells or 125I-albumin. Analysis of the outflow profiles indicated that hepatic artery perfusion did not affect transit time dispersion. However, heterogeneity of flow to individual portions of the liver, measured as the coefficient of variation, increased from 19 to 30%. These results indicate relatively uniform perfusion of the sinusoids in the portally perfused rat liver and that additional perfusion of the hepatic artery does not further improve hemodynamics. These results have significance for the design and interpretation of transport studies with the use of the perfused rat liver model.

Hepatocellular prolapse of hepatic portal tracts and subendothelial space of central veins in idiopathic portal hypertension

We report a case of idiopathic portal hypertension (IPH) with unusual liver pathology. The liver showed changes similar to these previously reported in IPH and, in addition, we observed the unusual features of prolapse of hepatocytes into portal tracts and also into the subendothelial space of hepatic veins. Hepatocyte prolapse into hepatic veins has previously been reported only in patients with a history of androgenic steroid therapy and immunosuppressive therapy. We speculate that, in our case, prolapse of hepatocytes could be related to the abnormal intrahepatic blood flow or to intrahepatic vasculopathy.

Intrahepatic portal blood flow dynamics in chronic liver disease; based on flow index involving liver size (In Japanese) : Yumiko S, Hiroaki S, Masato F, et al. (Department of Internal Medicine, Wakayama Medical College, Kihoku Hospital, 219 Myoji, Katsuragicho, Itogun, Wakayama 649-71, Japan). JPN J Med Imaging 1994;13:12–20

Intrahepatic portal blood flow dynamics in chronic liver disease; based on flow index involving liver size (In Japanese) : Yumiko S, Hiroaki S, Masato F, et al. (Department of Internal Medicine, Wakayama Medical College, Kihoku Hospital, 219 Myoji, Katsuragicho, Itogun, Wakayama 649-71, Japan). JPN J Med Imaging 1994;13:12–20

Human hepatic infarction: histopathological and postmortem angiological studies.

Twenty hepatic infarction cases selected from 5420 consecutive autopsy cases were investigated to clarify the pathogenetic aspects of this disease. Additional postmortem angiological studies of 24 normal human livers obtained at autopsy were also further performed to analyse the effects of blocking vascular structures on lesion development. Seventeen of the 20 cases (85%) were clinically associated with systemic circulatory insufficiency, especially hepato- and/or renal failure. Histopathologically, there was a significantly closer relationship between the location of infarcted regions and portal vein thrombosis than with either hepatic vein thrombosis or hepatic arterial damage. The borders between infarcted regions and surviving hepatic parenchyma were located around central veins, corresponding with the microcirculatory periphery of the portal venous system. Postmortem angiographic studies revealed that hepatic lobuli mainly consist of portal vein branches. Moreover, postmortem embolization studies of six normal livers using glass beads and barium-gelatin injection showed that physical occlusion of portal vein branches produced defects in broad areas of the hepatic parenchyma. Therefore, it is suggested that the development of hepatic infarction principally depends on disturbances of the portal venous system. In addition, systemic circulatory insufficiency, which reduces the intrahepatic blood flow, probably contributes greatly to the development of hepatic infarction.

Cellular and molecular aspects of hepatic fibrosis

Hepatic fibrosis, a consequence of most forms of chronic liver disease, is a dynamic process involving complex interactions between several cell types, the net result of which is accumulation of several distinct extracellular matrix (ECM) proteins. The resultant disruption of intrahepatic blood flow contributes to the development of portal hypertension. The effects, however, are not merely a space-occupying phenomenon; by changing the composition of the ECM, fibrosis may also alter hepatocyte function via cellular integrins. The principal source of ECM proteins in normal and fibrotic liver is the perisinusoidal cells which lie in the space of Disse. The response of this cell population to acute and chronic liver injury has been studied in detail. Perisinusoidal cells proliferate and become activated following hepatocyte necrosis. This phenomenon is transient in acute injuries, but in chronic liver disease, continued activation is associated with phenotypic modulation of perisinusoidal cells to myofibroblasts. This process is mediated by various cytokines including TGF-beta and PDGF. Some of the growth factors involved are derived from activated Kupffer cells and there is evidence of a complex interplay between mediators; injured sinusoidal endothelial cells and platelets are possible additional sources. Accumulation of ECM proteins in fibrosis can be explained not only by increased synthesis, but also by decreased degradation. There is growing evidence that in fibrotic liver there is decreased interstitial collagenase activity. This is, at least in part, due to expression of a tissue inhibitor of metalloproteinase, TIMP-1, by activated perisinusoidal cells.

Distribution of systemic blood flow in lambs with an aortopulmonary shunt during strenuous exercise.

We studied regional blood flows with radioactive-labeled microspheres in 12 7-wk-old lambs with an aortopulmonary left-to-right shunt [59 +/- 3% (SE) of left ventricular (LV) output] and in 11 control lambs, at rest and during exercise at 80% of predetermined peak O2 consumption. At rest, systemic blood flow was similar in the two groups. Blood flow to the heart and diaphragm was substantially higher in the shunt than in the control lambs. Blood flow to the other organs was not significantly different between the two groups. During exercise, systemic blood flow increased substantially but less in shunt (81%) than in control lambs (134%). Blood flow to the heart and diaphragm increased, that to the heart still being higher in shunt than in control lambs. Blood flow to the brain did not change, whereas that to the kidneys and splanchnic organs decreased to the same extent (25%) in shunt and control lambs. Intrahepatic and intrarenal blood flow redistribution in the shunt lambs persisted during exercise. In conclusion, myocardial blood flow is not increased at the expense of one particular organ, nor is it associated with an essential change in exercise-induced redistribution in shunt lambs.

Radiation Hepatology of the Rat: Microvascular Fibrosis and Enhancement of Liver Dysfunction by Diet and Drugs

Prior to whole-liver irradiation (0, 15, 25 Gy) rats were not treated, placed on a protein-deficient diet for 2 weeks, administered cyclophosphamide, and/or depleted of intracellular glutathione by injection with buthionine sulfoximide and diethyl maleate. At various times (0 to 84 days) after 0- and 25-Gy liver irradiation, liver function, liver mass, and hydroxyproline content were measured in nontreated animals. Liver function was measured in all other preirradiation regimens 2 to 3 months postirradiation. Histology and/or India ink perfusion of the liver were done on ascitic and jaundiced animals from all treatment groups. Approximately 20% of the 25-Gy whole-liver-irradiated animals in each preirradiation treatment group developed clinical signs of acute hepatitis (ascites, jaundice, and elevated liver enzymes in the plasma) 70 to 100 days after irradiation. Twenty-five-gray whole-liver irradiation also resulted in significant liver fibrosis that preceded the onset of liver dysfunction. Fibrotic changes were most dramatic in and around hepatic veins, sometimes resulting in complete or partial occlusion that disrupted intrahepatic blood flow and diminished liver function. In addition, a substantial accumulation of fluid in the liver of 25-Gy-irradiated livers occurred, resulting in a lower dry/wet liver weight ratio. Functional hepatic injury was enhanced by preirradiation treatment with a protein-deficient diet, cyclophosphamide, and/or depletion of intracellular glutathione. This enhancement of functional injury was pronounced after 15-Gy whole-liver irradiation when injury from radiation alone was minimal.

Computed tomography during arterial portography prior to transcatheter arterial therapy in hepatocellular carcinoma with marked portal extension: four case reports

Computed tomography during arterial portography (CTAP) is acknowledged as a valuable preoperative method for the detection of small intrahepatic lesions in patients with liver neoplasm. Four patients with hepatocellular carcinoma (HCC) with marked portal extension are presented. Evaluation of intrahepatic portal blood flow was achieved more accurately by CTAP than by conventional arterial portography. CTAP also plays an important role in patients with inoperable HCC, since portal extension is the most important prognostic factor of transcatheter arterial therapy.

Duplex sonography of hepatic artery thrombosis after liver transplantation.

When hepatic artery thrombosis occurs after liver transplantation, another transplantation is required to ensure the patient's survival. Because of the importance of establishing this diagnosis, we reviewed the results of duplex sonography in 37 angiographically or surgically proved cases of hepatic artery thrombosis after liver transplantation. There were 20 children and 17 adults. Ten of the 20 children had angiographically documented hepatopetal arterial collaterals. Such collaterals were not seen in the adult patients. This subset of patients was evaluated separately to determine if intrahepatic arterial blood flow reestablished by collaterals after hepatic artery thrombosis was a cause of false-negative Doppler studies. Thirty-four (92%) of the 37 cases of hepatic artery thrombosis were correctly identified by Doppler. A Doppler pulse was not identified in any of the children with arterial collaterals. We conclude that duplex sonography is sensitive in detecting hepatic artery thrombosis after liver transplantation. Furthermore, the presence of blood flow in hepatopetal arterial collaterals does not cause false-negative examinations.

Changes in the hepatic perfusion index during the growth and development of experimental hepatic micrometastases.

Micrometastases were induced in Fisher rats using an intraportal inoculation of 0.2 ml of 8 x 10(7) Walker carcinosarcoma cells. A control group received normal saline. The hepatic perfusion index (HPI) was measured during the growth and development of micrometastases. The HPI at 4 days (0.51 +/- 0.008) and at 6 days (0.65 +/- 0.16) was significantly raised when compared to controls (0.31 +/- 0.07) and at 2 days after inoculation (0.31 +/- 0.06). Hepatic artery flow did not change throughout the study period. However, portal venous inflow was decreased significantly at 4 and 6 days (0.57 +/- 0.16 and 0.55 +/- 0.11) when compared to controls (0.96 +/- 0.34). These results indicate that the change in the hepatic perfusion index is related to a decrease in portal venous inflow. The decrease in portal venous inflow could be a mechanical effect of the micrometastases on intrahepatic blood flow or to increased arteriovenous shunting.

Portal thrombosis: dynamic CT features and course.

Portal thrombosis was diagnosed on computed tomography (CT) in 10 patients and confirmed by sonography. CT demonstrated decreased density of the portal vessels in 9 patients with peripheral arterial concentration of contrast material surrounding the intraluminal thrombus. In 1 patient, a fresh thrombus was seen as an increase in intraluminal density on the pre-contrast scan. The involved vessels were generally enlarged. Three patients had follow-up scans, which revealed a cavernoma in 2 and complete patency of the portal vein and its branches following anticoagulant therapy in 1. In the latter patient, localized abnormal intra-hepatic blood flow suggested infarction of portal origin as the result of clot migration.

Smooth muscle in the hepatic artery, portal vein and hepatic vein within the liver of the raccoon and guinea pig

The amount and arrangement of smooth muscle in the intrahepatic vessels suggests that the guinea pig would be a good animal model for studying mechanisms controlling intrahepatic portal vein blood flow, while the raccoon would be good for studying hepatic vein mechanisms of control.

Heterogeneous intrahepatic distribution of blood flow in humans.

Color-functional imaging of intrahepatic blood flow was developed using the 133Xe clearance method and a gamma camera with a computer system. During the 2 min after intrasplenic injection of 133Xe in saline solution, 24 sequential gamma images were obtained. After setting the hepatic region, 133Xe clearance curves were extracted from the serial images every 6 X 6 mm element and regional blood flow for each element was calculated. The calculated regional hepatic blood flow values were displayed as a color images in eight color steps. Eleven patients with and without liver diseases were studied. In all the patients studied, heterogeneous intrahepatic distribution of blood flow was clearly demonstrated by the functional image of regional hepatic blood flow. Although a consistent pattern of intrahepatic distribution of blood flow was not obtained, greater-flow regions were frequently observed in the right lobe. Repeat studies in two patients demonstrated that the intrahepatic distribution of blood flow varied. The 10-15 s scintiphotosplenoportograms also showed the existence of restricted or preferential intrahepatic distribution of splenic flow. These results strongly suggest that intrahepatic distribution of blood flow in the human liver is heterogeneous and variable.

The vascular anatomy of the liver of the monitor lizard (Genus varanus).

AbstractThe gross and microscopic anatomy of the vasculature of the monitor lizard liver was studied. The portal vein has a peculiar arrangement of smooth muscle. The tunical media of the entering portal vein has bundles of smooth muscle cells separated by large numbers of collagenous fibers. The amount of smooth muscle decreases as the vessel decreases in diameter and soon one finds intermittent broad, thin bands of smooth muscle. As the caliber of the vessels continues to decrease, the smooth muscle bands become narrower and thicker so that they appear as doughnut‐shaped sphincters. The sphincters are usually found at the beginning of each branch of the portal vein as well as along the course of veins between areas of branching. Some sphincters are found in direct contact with the outer capsule of the liver. Sphincters occur in the terminal branches of the portal vein just proximal to the sinusoids.Small numbers of scattered smooth muscle cells were seen arranged longitudinally, obliquely, or circularly in the smaller hepatic veins. Even the large hepatic veins had only small amounts of smooth muscle. At no place along the course of hepatic veins could smooth muscle sphincters equivalent to those seen around portal veins be found.The monitor lizard should be an excellent subject for physiological and pharmacological studies of regulation of intrahepatic portal vein blood flow.

Intrahepatic distribution of hepatic blood flow: double-input studies

ARTICLESIntrahepatic distribution of hepatic blood flow: double-input studiesN Lifson, DG Levitt, Griffen WO Jr, and CJ EllisN Lifson, DG Levitt, Griffen WO Jr, and CJ EllisPublished Online:01 May 1970https://doi.org/10.1152/ajplegacy.1970.218.5.1480MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByBlood Flows in Tributaries of the Portal Vein: Anatomical and Angiographic Studies in Normal Beagle Dogs7 November 2014 | Anatomia, Histologia, Embryologia, Vol. 44, No. 6Heterogeneity of the intrahepatic portal venous blood flow: Impact on hepatocyte transplantationMicrovascular Research, Vol. 86PKQuest: volatile solutes – application to enflurane, nitrous oxide, halothane, methoxyflurane and toluene pharmacokinetics15 August 2002 | BMC Anesthesiology, Vol. 2, No. 1PKQuest: measurement of intestinal absorption and first pass metabolism – application to human ethanol pharmacokinetics15 August 2002 | BMC Clinical Pharmacology, Vol. 2, No. 1PKQuest: a general physiologically based pharmacokinetic model. Introduction and application to propranolol15 August 2002 | BMC Clinical Pharmacology, Vol. 2, No. 1PKQuest: capillary permeability limitation and plasma protein binding – application to human inulin, dicloxacillin and ceftriaxone pharmacokinetics26 September 2002 | BMC Clinical Pharmacology, Vol. 2, No. 1Dependency of the [18f]fluoromisonidazole uptake on oxygen delivery and tissue oxygenation in the porcine liverNuclear Medicine and Biology, Vol. 27, No. 8Use of a Two-Compartment Model to Assess the Pharmacokinetics of Human Ethanol MetabolismAlcoholism: Clinical and Experimental Research, Vol. 22, No. 8Measurement of liver blood flow using oxygen-15 labelled water and dynamic positron emission tomography: Limitations of model descriptionEuropean Journal of Nuclear Medicine, Vol. 23, No. 2Patterns of colorectal liver metastases according to Couinaud's segmentsDiseases of the Colon & Rectum, Vol. 38, No. 3Role of the hepatic artery in the metabolism of phenacetin and acetaminophen: An intravital microscopic and multiple-indicator dilution study in perfused rat liverHepatology, Vol. 20, No. 3Marked Heterogeneity in the Intrahepatic Distribution of Quinidine in Rats: Implications in PharmacokineticsJournal of Pharmaceutical Sciences, Vol. 79, No. 9Residence time distributions of solutes in the perfused rat liver using a dispersion model of hepatic elimination: 1. Effect of changes in perfusate flow and albumin concentration on sucrose and taurocholate1 June 1990 | Journal of Pharmacokinetics and Biopharmaceutics, Vol. 18, No. 3Liver blood flowGastroenterology, Vol. 81, No. 1Functional zones in rat liver: The degree of overlapJournal of Theoretical Biology, Vol. 89, No. 2Flow dependence of first-order uptake of substances by heterogeneous perfused organsJournal of Theoretical Biology, Vol. 86, No. 2Heterogeneity of macroscopic and single villus blood flow in rabbit small intestineMicrovascular Research, Vol. 17, No. 2The distribution of RB86 in different parts of the liverPfl�gers Archiv European Journal of Physiology, Vol. 346, No. 2 More from this issue > Volume 218Issue 5May 1970Pages 1480-1488 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.5.1480PubMed5438277History Published online 1 May 1970 Published in print 1 May 1970 Metrics

Effect of blood flow reversal in liver autotransplants upon the site of hepatocyte regeneration.

We studied the role of the direction of intrahepatic blood flow upon the location of hepatocyte formation in regenerating liver. Single liver lobes in the dog were autotransplanted to the region of the neck with the blood supply reestablished in a manner to perfuse the hepatic lobule from portal tract to central vein or, in a reverse direction, from central vein to portal tract. Partial resection of the nontransplanted liver was later performed to induce regeneration in the grafts by humoral means. Tritiated thymidine was administered, and radioautographs were prepared from excised graft and nontransplanted liver. In the "straight" blood flow grafts, as well as in all nontransplanted livers, labeled hepatocytes indicating DNA synthesis were found predominantly in the vicinity of the portal tracts. In the "reverse" blood flow grafts, labeled hepatocytes were more prevalent about the central veins. Thus, the localization of hepatocyte formation in the lobule during active liver regeneration cannot be attributed to an inherently greater capacity of periportal liver cells to divide but is probably related to their preferential exposure to blood constituent changes (humoral mechanisms). Hepatocyte regeneration in the presence of abnormal directional circulation might lead to lobular disorganization resulting in consequent biochemical aberrations despite the formation of new cells.