Peribiliary Capillary Plexus Research Articles

Movement of IgM antibody from blood to bile in rats

The movement from blood to bile of passively injected autologous IgM antibody against horse erythrocytes was studied in rats. Both native and neuraminidase-treated antibody entered bile intact, with the peak titers for both measured between 60 and 90 min after injection. A small part (0.38%) of the injected dose of native antibody and 1.05% of the asialo-IgM antibody appeared in bile over 24 hr. These recoveries represented only a small fraction of the activity, which apparently disappeared from serum over the period. The pathways used by IgM antibody to enter bile were partially assessed. Prior injection of fetuin was found to abrogate the biliary secretion of native antibody and to significantly reduce the recovery of asialoantibody in bile. In contrast, the presence of asialofetuin reduced (but not significantly) the secretion of native antibody and markedly changed the kinetics of appearance of asialo-IgM activity in bile. Some candidate routes to bile can be excluded as unlikely. The parahepatocellular pathway to bile canaliculi appears uninvolved because the secretion of antibody is slow and the inhibitory effects of fetuin argue against secretory component-mediated transport. Instead, two secretory pathways appear to be present. The first appears to be available to both native and asialo-IgM antibody, and may involve the peribiliary capillary plexus. The second route to bile is available to asialo-IgM antibody alone and is probably initiated by binding to the hepatic asialoglycoprotein receptor.

Bovine probursin tetradecapeptide contains amino acid sequence from somatostatin, tuftsin and bursin.

The B cell differentiating tripeptide bursin (lysyl-histidyl-glycyl-amide) is found in avian and mammalian bone marrow and in epithelial cells of the avian bursa of Fabricius and mammalian intrahepatic bile ducts. We now report the structure of probursin (Phe-Phe-Trp-Lys-Thr-Lys-Pro-Arg-Lys-His-Gly-Gly-Arg-Arg) isolated from bovine bone marrow and liver. Amino acids 1-5 correspond to the active site of somatostatin, 5-8 to tuftsin and 9-11 to bursin. Intact probursin has the biological activity of both somatostatin and bursin, and known enzyme cleavages could release free tuftsin, although intact probursin has low tuftsin activity. Probursin and its component peptides could regulate other bone marrow functions in addition to B cell differentiation, and, in mammals, could also regulate the function of hepatocytes and Kupffer cells after transport to the hepatic sinusoids via a local portal system involving the peribiliary capillary plexus.

ラット肝・胆管血管鋳型の走査電顕像

Microvascular features of normal rat livers and bile duct system were examined with the vascular casts using methacrylated resin. Portal vein branches not only showed regular tapered down bifurcations but also had many side branches, some of which were directly connected with sinusoids. Terminations of hepatic arterial branches were divided into three types: 1) Many branches pouring into peribiliary capillary plexus (PBP), 2) branches directly pouring into periportal sinusoids and/or peripheral portal vein branches via arterio-portal anastomoses, and 3) anastomoses with periportal vascular plexus. PBP was composed of rich vascular networks. In large portal tracts, the plexus showed two layers, that is, the inner layer made up of a close network of capillary vessels and the outer layer consisting of a loose network of arteries and veins, while the PBP in the small portal tracts was composed of only a single layer of loose capillary network. Transitional features of these two patterns were found in the medium-sized portal tracts. PBP was supplied by afferent vessels from the interlobular hepatic artery as described above, and were directly connected with interlobular branches of the portal vein (internal root). The extrahepatic bile duct revealed a much richer vasculature than the intrahepatic bile duct. Both arterial and venous branches were ramified at almost right angle from a pair of arteries and veins running parallel with the bile duct. Occasional strictures, which might have been sphincter portions of the media, were noted at the branching sites of the artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Microvasculature in the small portal tracts in idiopathic portal hypertension

The morphology of the microvasculature in the small portal tracts was examined in normal livers, idiopathic portal hypertension (IPH) and other hepatic diseases. The microvasculature examined was arbitrary divided into two groups: that near the limiting plate and that within portal tracts, particularly around bile ducts. Based on comparisons of histology, immunohistochemistry and vascular casts, it is suggested that the former corresponded to inlet venules and the latter to distributing portal veins and peribiliary capillary plexus. Both of these microvasculatures were positive for Ulex europaeus lectin I, and (infrequently and weakly) for factor VIII-related antigen. Morphometry disclosed that inlet venules were reduced in number in IPH compared with normal livers and that distributing portal veins, peribiliary capillary plexus and inlet venules were increased in extrahepatic portal obstruction, chronic active hepatitis and extrahepatic obstructive cholestasis. We believe that the change in the microvasculature reflects abnormal microcirculation in the small portal tracts, and that the reduction of inlet venules plays an important role in the development of portal hypertension in IPH.

Histological and ultrastructural examination of the intrahepatic biliary tree in primary sclerosing cholangitis.

Intrahepatic bile ducts were examined histologically and ultrastructurally in wedge-biopsied liver specimens from three patients with primary sclerosing cholangitis. Bile ducts with periductal concentric fibrosis, which is a characteristic finding in primary sclerosing cholangitis, revealed ultrastructurally finger-like projections or fine undulations of the basal free surfaces with markedly duplicated basal lamina. The lamina was collared by a layer of elongated fibroblasts and thickened bundles of collagen fibers outwards. These changes were consistently found in all sizes of ducts examined, and might be related to progressive periductal fibrosis. Serial section observations showed that some severely affected ducts actually disappeared when accompanying severe periductal fibrosis. It would therefore appear that progressive periductal fibrosis may interrupt fluid and nutrient exchange between the bile duct epithelia and peribiliary capillary plexus, followed by obliteration of the biliary lumina. Although the bile ducts showed segmentally periductal lymphocytic infiltration and, ultrastructurally, point contacts between infiltrating lymphocytes and biliary epithelial cells were observed occasionally, the exact role of infiltrating lymphocytes in the pathogenesis of primary sclerosing cholangitis remains unclear.

Intrahepatic circulation in liver disease.

Using the multiple indicator dilution approach, events occurring in the microvascular bed can be characterized in experimental animals with different types of cirrhosis and in man. Intrahepatic shunts can be found shunting blood away from sinusoids in both cirrhotic patients and cirrhotic animals. Such shunts were present in about one-third of cirrhotic patients with portal hypertension, and occurred mainly between the portal vein and hepatic veins. In cirrhotics, portohepatic anastomoses are usually large in diameter (more than 20 micron in diameter). Collagenization of the space of Disse and the progressive transformation of sinusoids into capillary-like channels decrease the extravascular space accessible to albumin and probably to other large molecules and protein-bound substances. However, unlike findings obtained in well-capillarized organs, these sinusoidal changes do not appear to limit the diffusion of sucrose, water, and lipophilic substances, such as lidocaine in the extravascular and intracellular spaces. The pattern observed for labeled sucrose curves following hepatic artery injection in cirrhotic patients could be secondary to the passage through the dense peribiliary capillary plexus originating from the enlarged arterial bed in cirrhosis. The difference in the perfusion of cirrhotic nodules with regard to the portal venous and hepatic artery routes introduces important new concepts in the overall mechanism of the elimination of endogenous and exogenous substances by the cirrhotic liver: blood entering the liver by the two afferent vessels will not flow through the same vascular bed before reaching the efferent hepatic veins.

The terminal distribution of the hepatic artery and its relationship to the development of focal liver necrosis following interruption of the portal blood supply.

The terminal distribution of the hepatic artery of the human liver was examined by arterial injection of india ink and serial sectioning. The branches of the hepatic artery form capillary networks around the bile duct in the portal tract, from which the capillaries (terminal venous branch) arise and connect with sinusoids at the most peripheral zone of the liver lobules. Evidence of direct anastomosis between the hepatic artery and portal vein inside the portal tract or presence of “innere Pfortaderwurzeln” as well as the intralobular arteriole was not demonstrated.The authors also studied the hepatic changes caused by interruption of the portal blood supply to the liver lobule. It was demonstrated that the portal tract and its components as well as several layers of liver parenchymal tissue around the portal tract are nourished from blood via the peribiliary capillary plexus and thus remains unaffected by portal obstruction, while other parts of the liver lobule will undergo coagulation necrosis.Based on the present investigation, the authors believe that the hepatic artery plays the main role in the nourishment of the bile duct while it has little to do with that of the liver lobule, except for the most peripheral layers of the liver lobules adjacent to the portal areas.