Effects of Perfusate on Cation Transport by Slices from the Isolated Perfused Rat Liver

1972 ◽  
Vol 50 (9) ◽  
pp. 916-919
Author(s):  
A. C. Nestruck ◽  
R. W. Furneaux
Keyword(s):  
Red Blood Cells ◽  
Rat Liver ◽  
Blood Cells ◽  
Liver Perfusion ◽  
Isolated Perfused Rat Liver ◽  
Buffer Solution ◽  
Bicarbonate Buffer ◽  
Rat Liver Perfusion ◽  
Metabolic Substrates ◽  
Perfusion Studies

Isolated livers from fed rats were perfused for 1 h with a basic Krebs–Ringer bicarbonate buffer solution containing albumin and glucose and added (1) α-ketoglutarate, (2) pyruvate, fumarate, and glutamate, or (3) washed red blood cells. Perfusate flow rate, [Formula: see text], [Formula: see text], and pH changes across the liver, and glucose efflux in the perfusate, were measured during perfusion. Rewarmed slices of liver taken at the beginning of perfusion were found to be able to reverse a cation shift imposed by cold incubation. Slices of liver taken after 1 h of perfusion were not able to effect this cation shift unless red blood cells were included in the perfusate. It is proposed that noncellular perfusates containing metabolic substrates are not ideal for isolated rat liver perfusion studies as evidenced in the altered membrane transport capacity of slices after perfusion.

A compartmental model for bilirubin kinetics in isolated perfused rat liver

1976 ◽  
Vol 54 (3) ◽  
pp. 277-286 ◽  
Author(s):  
M. Sawkat Anwer ◽  
Ronald Gronwall
Keyword(s):  
Red Blood Cells ◽  
Rat Liver ◽  
Blood Cells ◽  
Compartmental Model ◽  
Current Knowledge ◽  
Compartment Model ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Perfusion Apparatus ◽  
Bilirubin Binding

Bilirubin kinetics were studied in an isolated, perfused rat liver system using unconjugated [14C]bilirubin (UC[14C]B) and Δ-amino[4-14C]levulinic acid (A[14C]LA) to derive a suitable compartmental model. Plasma disappearance of UC[14C]B, plasma appearance of conjugated [14C]bilirubin (C[14C]B) and biliary excretion of C[14C]B were followed for 90–120 min following injection of UC[14C]B. Hepatic content of labeled bilirubin 12 min after the injection of UC[14C]B was determined directly in five separate perfusion experiments. UCB was found to reflux back to plasma from liver in two experiments using A[14C]LA. Bilirubin binding to red blood cells (6–8% of the perfusate level) and the components of the perfusion apparatus (4–6% of perfusate level) was estimated by performing a control experiment without the liver. A six compartment model was necessary and adequate to explain the experimental data and current knowledge of bilirubin metabolism: (1) UCB bound to red blood cells and the perfusion apparatus, (2) plasma UCB, (3) liver UCB, (4) liver CB, (5) plasma CB, and (6) bile CB. The proposed model could serve as a reference point for studies of bilirubin kinetics in whole animals for normal and abnormal states.

[14C]urea and 58Co-EDTA as reference indicators in hepatic multiple indicator dilution studies

1990 ◽  
Vol 259 (1) ◽  
pp. G32-G40 ◽  
Author(s):  
K. S. Pang ◽  
F. Barker ◽  
A. J. Schwab ◽  
C. A. Goresky
Keyword(s):  
Molecular Weight ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Liver Perfusion ◽  
Indicator Dilution ◽  
Space Distribution ◽  
Low Molecular Weight ◽  
Multiple Indicator Dilution ◽  
Perfusion Studies ◽  
Multiple Indicator

The space distribution and the processes underlying uptake of tracer substrate may be appraised by the multiple indicator dilution technique, after the simultaneous injection of noneliminated vascular (51Cr-labeled red blood cells), extracellular (125I-labeled albumin and [14C]sucrose for high and low molecular weight interstitial space, respectively), and cellular (3H2O) indicators and tracer substrate. When tracer substrates and/or their metabolites containing 14C or 3H labels are being studied, it becomes necessary to find substitutions for the similarly labeled noneliminated indicators. In red blood cell-perfused rat livers, 58Co-EDTA is found to be a good replacement for the low molecular weight interstitial reference; it has a space distribution indistinguishable from that for [14C]sucrose. [14C]urea and 3H2O, which distribute similarly in red blood cells, have similar outflow dilution profiles. With corrections for minor deviations in recovery [a ratio of 0.936 +/- 0.024 (SD)] and transit time [a ratio of 0.962 +/- 0.008 (SD)], the cellular water space can be closely approximated from the [14C]-urea curve. 58Co-EDTA and [14C]urea are reasonable substitutes for [14C]sucrose and 3H2O, respectively, in multiple indicator dilution liver perfusion studies for investigating transfer and removal characteristics of tracer substrates.

An Optimized Model for Rat Liver Perfusion Studies

1996 ◽  
Vol 66 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Kee Cheung ◽  
Peter E. Hickman ◽  
Julia M. Potter ◽  
Neal I. Walker ◽  
Megan Jericho ◽  
...  
Keyword(s):  
Rat Liver ◽  
Liver Perfusion ◽  
Rat Liver Perfusion ◽  
Perfusion Studies ◽  
Optimized Model

Bioanalytical Method Validation of an RP-HPLC Method for Determination of Rifampicin in Liver Perfusion Studies

2020 ◽  
Vol 16 ◽  
Author(s):  
Nihan Izat ◽  
Ozan Kaplan ◽  
Mustafa Celebier ◽  
Selma Sahin
Keyword(s):  
Method Validation ◽  
Rat Liver ◽  
Liver Tissue ◽  
Liver Perfusion ◽  
Bioanalytical Method Validation ◽  
Bioanalytical Method ◽  
Rat Liver Perfusion ◽  
Perfusion Studies ◽  
Carry Over

Background: The number of validated quantification methods for rifampicin, a prototypical Oatp inhibitor, in biological rat samples was limited. Objective: This study was conducted to validate a modified reversed-phase liquid chromatographic method for the determination of rifampicin in rat liver tissue according to the current ICH M10 Bioanalytical Method Validation Draft Guideline (2019) for application to samples of in situ rat liver perfusion studies. Method: Liver tissue samples were obtained from recirculatory in situ rat liver perfusion studies. The analysis was performed on a C18 column with a mobile phase composed of 0.05 M phosphate buffer (pH 4.58): acetonitrile (55:45, v/v). The assay was validated for selectivity, calibration curve and range, matrix effect, carry-over, accuracy and precision, reinjection reproducibility, and stability. Results: The method was considered selective and stable, without having carry-over and matrix effects. The calibration curve was linear (R2: 0.9983) within the calibration range (0.5-60 ppm). Accuracy and precision values fulfilled the required limits. Liver concentrations of rifampicin in liver tissue, obtained after 60 min perfusion with 10 µM and 50 µM of rifampicin were 45.1 ± 11.2 and 313.4 ± 84.4 µM, respectively. Conclusion: The bioanalytical method validation was completed and the method was successfully applied for the determination of rifampicin in rat liver tissue.

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.

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