Hepatic Microcirculation in Hemorrhagic Shock1

2015 ◽  
pp. 85-105 ◽  
Author(s):  
Brigitte Vollmar ◽  
M. D. Menger ◽  
G. Lang ◽  
S. Post ◽  
K. Messmer
Keyword(s):  
Hepatic Microcirculation

Metalloporphyrins, used for HO-1 Inhibition, Themselves Affect Hepatic Microcirculation, Liver Function, and Hepatocellular Integrity

2009 ◽  
Vol 16 (4) ◽  
pp. 355-363 ◽  
Author(s):  
Stefan Scheingraber ◽  
Sven Messner ◽  
Susanne Matt ◽  
Kathrin Abel ◽  
Simone Goger ◽  
...  
Keyword(s):  
Liver Function ◽  
Hepatic Microcirculation

Short-term treatment with hepatoselective NO donor V-PYRRO/NO improves blood flow in hepatic microcirculation in liver steatosis in mice

2018 ◽  
Vol 70 (3) ◽  
pp. 463-469 ◽  
Author(s):  
Edyta Kus ◽  
Krzysztof Jasiński ◽  
Tomasz Skórka ◽  
Izabela Czyzynska-Cichon ◽  
Stefan Chlopicki
Keyword(s):  
Blood Flow ◽  
Liver Steatosis ◽  
Term Treatment ◽  
Short Term ◽  
Short Term Treatment ◽  
Hepatic Microcirculation ◽  
No Donor

Endogenous ET-1 contributes to liver injury induced by galactosamine and endotoxin in isolated perfused rat liver

1995 ◽  
Vol 268 (6) ◽  
pp. G997-G1003 ◽  
Author(s):  
T. Ohuchi ◽  
K. Tada ◽  
K. Akamatsu
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Early Event ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Hepatic Microcirculation ◽  
Nonparenchymal Cells ◽  
Multiple Indicator Dilution ◽  
Microcirculatory Disturbances ◽  
Hepatocyte Damage

Injury to hepatocytes most likely occurs via disturbances in the microcirculation. The role of vasoconstriction due to the effect of endogenous endothelin-1 (ET-1) in the development of galactosamine (GalN)- and lipopolysaccharide (LPS)-induced liver injury was investigated. Using the multiple indicator dilution technique, we measured the volume of the hepatic sinusoids and the apparent Disse space as indicators of overall hepatic microcirculation. Serum purine nucleoside phosphorylase activity as a marker of damage to nonparenchymal cells increased and the volume of the sinusoids and the Disse space decreased prior to hepatocyte damage in rats treated intraperitoneally with GalN and LPS. Moreover, the amount of ET-1 release was elevated. When livers from untreated rats were perfused with ET-1 in a recirculating system, hepatocyte damage was observed similar to experiments with GalN and LPS. A monoclonal anti-endothelin antibody, AwETN40, diminished the extent of liver injury caused by GalN and LPS in isolated perfused rat liver. The present study suggests that vasoconstriction is an early event in GalN- and LPS-induced liver injury and that the development of hepatocyte damage is mediated via microcirculatory disturbances due to endogenous ET-1.

scholarly journals Hepatic Microcirculation in Fatty Liver Disease

2008 ◽  
Vol 291 (6) ◽  
pp. 684-692 ◽  
Author(s):  
Geoff C. Farrell ◽  
N.C. Teoh ◽  
R.S. Mccuskey
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Hepatic Microcirculation

Effects of oxidized low-density lipoproteins on the hepatic microvasculature

2011 ◽  
Vol 301 (4) ◽  
pp. G684-G693 ◽  
Author(s):  
Ana Oteiza ◽  
Ruomei Li ◽  
Robert S. McCuskey ◽  
Bård Smedsrød ◽  
Karen Kristine Sørensen
Keyword(s):  
Electron Microscopy ◽  
Linear Trend ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Intercellular Adhesion Molecule ◽  
Organ Distribution ◽  
Low Density ◽  
Hepatic Microcirculation ◽  
Oxidized Low Density Lipoproteins

Oxidized low-density lipoproteins (oxLDLs) are involved in proinflammatory and cytotoxic events in different microcirculatory systems. The liver is an important scavenger organ for circulating oxLDLs. However, the interaction of oxLDL with the hepatic microcirculation has been poorly investigated. The present study was conducted to examine the effects of differently modified oxLDLs on the hepatic microvasculature. C57Bl/6J mice were injected intravenously with low-density lipoprotein (LDL), or LDL oxidized for 3 h (oxLDL3) or 24 h (oxLDL24), at doses resembling oxLDL plasma levels in cardiovascular disease patients. Radioiodinated ligands were used to measure blood decay and organ distribution, and nonlabeled ligands to evaluate microcirculatory responses, examined by in vivo microscopy 30–60 min after ligand injection, immunohistochemistry, and scanning and transmission electron microscopy. Mildly oxLDL (oxLDL3) was cleared from blood at a markedly slower rate than heavily oxLDL (oxLDL24), but significantly faster than LDL ( P < 0.01). Injected oxLDLs distributed to liver. OxLDL effects were most pronounced in central areas of the liver lobules where oxLDL3elicited a significant ( P < 0.05) reduction in perfused sinusoids, and both oxLDL3and oxLDL24significantly increased the numbers of swollen endothelial cells and adherent leukocytes compared with LDL ( P < 0.05). OxLDL-treated livers also exhibited increased intercellular adhesion molecule (ICAM)-1 centrilobular staining. Electron microscopy showed a 30% increased thickness of the liver sinusoidal endothelium in the oxLDL3group ( P < 0.05) and a reduced sinusoidal fenestration in centrilobular areas with increased oxidation of LDL ( P for linear trend <0.05). In conclusion, OxLDL induced several acute changes in the liver microvasculature, which may lead to sinusoidal endothelial dysfunction.

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