scholarly journals Oestradiol 17β-glucuronide increases tight-junctional permeability in rat liver

1989 ◽  
Vol 261 (1) ◽  
pp. 297-300 ◽  
Author(s):  
K S Kan ◽  
M J Monte ◽  
R A Parslow ◽  
R Coleman
Keyword(s):  
Rat Liver ◽  
Bile Flow ◽  
Liver Perfusion ◽  
Single Pulse ◽  
Peak Height ◽  
Acute Administration ◽  
Flow Rates ◽  
Rat Liver Perfusion ◽  
Junctional Permeability ◽  
Bile Acid Secretion

By using rat liver perfusion under one-pass conditions with a single pulse of horseradish peroxidase (HRP), the biliary output of HRP was used as an indicator of paracellular permeability change caused by the cholestatic compound oestradiol 17 beta-glucuronide (E17G). Since E17G reduced bile flow, we have also used, during the assessment of junctional permeability after E17G treatment, the choleretic compound taurodehydrocholate to enhance bile flow back to control levels. At both low and restored bile flow rates, the acute administration of E17G (3.4 mumol) increased the HRP peak height, thereby indicating that one of the hepatotoxic actions of E17G is to increase the permeability of hepatic tight junctions. The action of E17G in affecting bile acid secretion and biliary volume are also explored.

scholarly journals The calcium ionophore A23187 increases the tight-junctional permeability in rat liver

1988 ◽  
Vol 256 (3) ◽  
pp. 1039-1041 ◽  
Author(s):  
K S Kan ◽  
R Coleman
Keyword(s):  
Horseradish Peroxidase ◽  
Rat Liver ◽  
Bile Flow ◽  
Calcium Ionophore ◽  
Peak Height ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Hepatocellular Damage ◽  
Junctional Permeability ◽  
Second Peak

The effect of an increase in intracellular Ca2+ concentration on tight-junctional permeability in rat liver was studied by using the calcium ionophore A23187. Infusion of 100 microliters of dimethyl sulphoxide containing various amounts of A23187 over 30 min into isolated perfused livers was followed by a pulse of horseradish peroxidase (HRP) under single-pass conditions. The first biliary HRP peak, a measure of junctional permeability, was increased 4-fold with 100 micrograms of A23187. There were, however, no significant effects on bile flow or on aspartate aminotransferase leakage as compared with the control at this dosage, and thus the increase in junctional permeability was occurring without evidence of appreciable cholestatic or hepatocellular damage. Higher dosages of A23187, however, caused not only an increase in HRP peak height but also changes in bile flow and increases in aminotransferase leakage, indicating more extensive effects at these higher dosages. A second peak of HRP secretion, occurring 20-25 min after the HRP pulse, was also elevated approx. 3.5-fold; this may indicate that pinocytosis and transcellular movement of HRP are also increased under these conditions.

scholarly journals Alterations of lysosomal size and density during rat liver perfusion. Suppression by insulin and amino acids.

1977 ◽  
Vol 252 (19) ◽  
pp. 6948-6954 ◽  
Author(s):  
A N Neely ◽  
J R Cox ◽  
J A Fortney ◽  
C M Schworer ◽  
G E Mortimore
Keyword(s):  
Amino Acids ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Rat Liver Perfusion

A flowmeter for use in monitoring oxygen uptake in rat liver perfusion

1967 ◽  
Vol 5 (4) ◽  
pp. 347-352 ◽  
Author(s):  
A. J. Barak ◽  
H. C. Beckenhauer ◽  
R. A. Myers ◽  
R. N. Wilger
Keyword(s):  
Oxygen Uptake ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Rat Liver Perfusion

scholarly journals Portal hypertensive response to kinin

2009 ◽  
Vol 81 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Maria Kouyoumdjian ◽  
Marcia R. Nagaoka ◽  
Mauricio R. Loureiro-Silva ◽  
Durval R. Borges
Keyword(s):  
Vascular Resistance ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Stellate Cells ◽  
Kinin System ◽  
Rat Liver Perfusion ◽  
Isolated Liver Cells ◽  
B2 Receptors ◽  
Intrahepatic Vascular Resistance

Portal hypertension is the most common complication of chronic liver diseases, such as cirrhosis. The increased intrahepatic vascular resistance seen in hepatic disease is due to changes in cellular architecture and active contraction of stellate cells. In this article, we review the historical aspects of the kallikrein-kinin system, the role of bradykinin in the development of disease, and our main findings regarding the role of this nonapeptide in normal and experimentalmodels of hepatic injury using the isolated rat liver perfusion model (mono and bivascular) and isolated liver cells. We demonstrated that: 1) the increase in intrahepatic vascular resistance induced by bradykinin is mediated by B2 receptors, involving sinusoidal endothelial and stellate cells, and is preserved in the presence of inflammation, fibrosis, and cirrhosis; 2) the hepatic arterial hypertensive response to bradykinin is calcium-independent and mediated by eicosanoids; 3) bradykinin does not have vasodilating effect on the pre-constricted perfused rat liver; and, 4) after exertion of its hypertensive effect, bradykinin is degraded by angiotensin converting enzyme. In conclusion, the hypertensive response to BK is mediated by the B2 receptor in normal and pathological situations. The B1 receptor is expressed more strongly in regenerating and cirrhotic livers, and its role is currently under investigation.

Uridine regulation by the isolated rat liver: perfusion with an artificial oxygen carrier

1982 ◽  
Vol 242 (5) ◽  
pp. R465-R470 ◽  
Author(s):  
A. Monks ◽  
R. L. Cysyk
Keyword(s):  
Rat Liver ◽  
Oxygen Carrier ◽  
Liver Perfusion ◽  
Blood Substitute ◽  
Rat Plasma ◽  
Perfusion Medium ◽  
Artificial Oxygen Carrier ◽  
Isolated Rat Liver ◽  
Rat Liver Perfusion ◽  
Isolated Rat

The isolated rat liver was used to investigate the role of the liver in the regulation of circulating uridine concentrations. A synthetic blood substitute (Fluosol-43) was utilized as an alternative oxygen-carrying perfusion medium to a simplified blood preparation and produced no apparent hepatotoxicity within the perfusion period. The isolated rat liver excreted uridine into a circulating perfusion medium achieving concentrations similar to those found in rat plasma (1.4 +/- 0.6 microM). The mean output of uridine over 2 h was 107 nmol.h-1.g liver-1, but if the perfusate was recirculated the net output of uridine was reduced to 12.7 nmol.h-1.g-1. The rate of depletion of nonphysiological concentrations of circulating uridine was found to be concentration dependent up to 25 microM. At a steady state of circulating uridine, a radioactive uridine spike was cleared with a half-life of 7.4 min and an elimination constant of 0.094 min-1; 30% of the radioactivity appeared in the perfusate as metabolites of uridine within 40 min. Thus the perfused rat liver acts to maintain circulating uridine concentrations similar to those measured in plasma.

Etude du métabolisme du 3-propyl-éther de l'estradiol 17β comparativement à l'estradiol 17β dans le foie de rat perfusé

1978 ◽  
Vol 56 (10) ◽  
pp. 985-992 ◽  
Author(s):  
Jean-Pierre Tresca ◽  
Geneviève Ponsard ◽  
Hervé Degrelle ◽  
Max-Fernand Jayle
Keyword(s):  
Rat Liver ◽  
Liver Perfusion ◽  
Ether Group ◽  
Experimental Conditions ◽  
Active Uptake ◽  
Rat Liver Perfusion ◽  
Constant Rate ◽  
Enzymatic Systems

The metabolism of 6,7-3H-tabelled 3-propyl ether estradiol (PE2) and of [6,7-3H]estradiol was studied by rat liver perfusion under different experimental conditions. In all cases, 90% of the radioactivity was retained in the liver, indicating an active uptake by the liver. The hepatic radioactivity was slowly released at a constant rate in the efferent perfusate. The proportion of radioactive metabolites in the perfusate was approximately the same as in the liver.3-Propyl ether estrone (PE1), a dehydrogenation product of PE2, and 3-propyl ether estriol (PE3), a 16α-hydroxylated derivative of PE2, were identified. Propylated metabolites more polar than PE2 were found. A low amount of propylated metabolites was conjugated with the exception of PE1. From the appearance of phenolic steroids including estrone, estradiol, and estriol, it was concluded that cleavage of the 3-propyl ether group had occurred.Compared with perfusion under oxygen, the overall metabolism was significantly reduced when the perfusion was carried out under nitrogen which demonstrates that oxygen plays a part in all the enzymatic systems involved. When animals were stimulated by phenobarbital, their entire metabolism was activated. These results suggest a metabolism mainly located in the hepatic microsomes.Our results show that the propylated hormone is metabolized like the free hormone. However, the transformations of PE2 are slower when compared with estradiol: thus, the 3-propyl ether group provided some hormone protection against hepatic degradation.

Attenuation of hepatic microcirculatory failure during in situ xenogeneic rat liver perfusion by heat shock preconditioning

2000 ◽  
Vol 32 (5) ◽  
pp. 1111 ◽  
Author(s):  
H Terajima ◽  
A Thiaener ◽  
C Hammer ◽  
K Messmer ◽  
Y Yamamoto ◽  
...  
Keyword(s):  
Heat Shock ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Rat Liver Perfusion
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