Effect of Allylisopropylacetamide on the Conversion of Heme (Ferriprotoporphyrin IX) to Bilirubin in Rat Liver Perfusion in vitro

2015 ◽  
pp. 80-85
Author(s):  
H. H. Liem ◽  
U. Muller-Eberhard
Keyword(s):  
Rat Liver ◽  
Liver Perfusion ◽  
Rat Liver Perfusion

scholarly journals Evaluation for effect of hypothermia on the disposition of 4-nitrophenol in rats by in-vitro metabolism study and rat liver perfusion system

2013 ◽  
Vol 65 (10) ◽  
pp. 1536-1540 ◽  
Author(s):  
Hirotaka Miyamoto ◽  
Satoshi Matsueda ◽  
Kotaro Komori ◽  
Shintaro Fumoto ◽  
Mikiro Nakashima ◽  
...  
Keyword(s):  
Rat Liver ◽  
Liver Perfusion ◽  
In Vitro Metabolism ◽  
Perfusion System ◽  
Rat Liver Perfusion ◽  
Metabolism Study

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.

The disappearance rate of human versus rat intermediate density lipoproteins from rat liver perfusion

1991 ◽  
Vol 69 (8) ◽  
pp. 537-543 ◽  
Author(s):  
Robert Dupras ◽  
Louise Brissette ◽  
Paul D. Roach ◽  
Sylvain Begin ◽  
André Tremblay ◽  
...  
Keyword(s):  
Liver Perfusion ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Disappearance Rate ◽  
Very Low Density Lipoproteins ◽  
Rat Liver Perfusion ◽  
Heparin Plasma ◽  
Intermediate Density

The aim of this work was to compare the disappearance rate of human and rat intermediate density lipoproteins (IDL) using the rat liver perfusion system. Human and rat IDL were produced in vitro by incubating human or rat very low density lipoproteins (VLDL) with either rat post-heparin plasma (method I) or a resolubilized isopropanol precipitate of rat post-heparin plasma (method II). With both methods, the degree of triacylglycerol lipolysis was approximately 55%. The different preparations of IDL were labelled with 125I and added to perfusates of rat livers. The disappearance rates of 125I-labelled IDL were monitored by measuring the radioactivity associated with apolipoprotein (apo) B in the perfusate during a 15-min period. Both human and rat IDL prepared with method I had an increased apoE to apoC ratio as compared with their native counterparts. Furthermore, human IDL had a significantly higher apoE to apoC ratio than rat IDL. However, when IDL were produced in the absence of exchangeable apolipoproteins (method II), no change in the apoE to apoC ratios was observed for the transformation of VLDL to IDL and the ratios were similar for human and rat IDL. Despite these differences, human IDL were always removed at a lower rate than rat IDL. The only striking difference between the two types of IDL made by method II was that the apoB100 to apoB48 ratio was considerably higher in human than in rat IDL. These results suggest that the apoB100 to apoB48 ratio is likely to be responsible for the observed differences in liver uptake between rat and human IDL.Key words: very low density lipoproteins, intermediate density lipoproteins, low density lipoproteins, hepatic lipoprotein receptors, intermediate density lipoprotein uptake, in vitro lipolysis, very low density lipoprotein remnants, apolipoproteins.

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.

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