Imipramine Kinetics in the Single Pass Rat Liver Perfusion Model

2009 ◽  
Vol 50 (2) ◽  
pp. 137-147 ◽  
Author(s):  
Erland J. Erlandsen ◽  
Lars F. Gram
2018 ◽  
Vol 102 (5) ◽  
pp. e205-e210 ◽  
Author(s):  
Federica Rigo ◽  
Nicola De Stefano ◽  
Victor Navarro-Tableros ◽  
Ezio David ◽  
Giorgia Rizza ◽  
...  

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

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

2009 ◽  
Vol 81 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Maria Kouyoumdjian ◽  
Marcia R. Nagaoka ◽  
Mauricio R. Loureiro-Silva ◽  
Durval R. Borges

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.


1982 ◽  
Vol 242 (5) ◽  
pp. R465-R470 ◽  
Author(s):  
A. Monks ◽  
R. L. Cysyk

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.


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