scholarly journals Euro-Collins Solution Versus Uw-Solution for Long-Term Liver Preservation in the Isolated Rat-Liver Perfusion Model

HPB Surgery ◽  
1991 ◽  
Vol 4 (4) ◽  
pp. 313-320 ◽  
Author(s):  
René Den Toom ◽  
Marion De Jong ◽  
Eric P. Krenning ◽  
Hans J. Van Der Hoek ◽  
Fiebo J. W. Ten Kate ◽  
...  

To compare UW-solution (UW) and Euro-Collins (EC) for long-term liver preservation we investigated the morphology and metabolic capacity of rat liver after 18 and 42-hours cold-storage in either UW or EC.After harvesting the rat liver was transferred to a perfusion chamber where it was perfused for 10 min with UW or EC at 4°C. Thereafter livers were stored at 4°C in UW or EC for 18 hours (both groups n = 6) or for 42 hours (both groups n = 8). After 18-hr or 42-hr cold-storage a 2-hr warm perfusion (37°C) was started with Krebs-Ringer solution with carbogen to which 125Iodine-triiodothyronine (T3) was added. Control livers (n = 8) were immediately perfused with Krebs-Ringer without cold-storage. The following parameters were assessed: ASAT-levels in the perfusate, T3-metabolites in the bile and the perfusate, the perfusion pressure, the volume of bile secreted and light-microscopical morphology at the end of the warm perfusion period.After cold storage in UW-solution the ASAT-levels in the perfusate were lower than after storage in EC as well as the perfusion pressures. These livers demonstrated a better T3-metabolism and secreted more bile than EC-stored livers. Histological examination showed more tissue damage in the EC-stored livers than in the UW stored livers.We conclude that cold-storage of rat liver in UW-solution resulted in a better morphology and metabolic capacity as compared with EC-solution.

Cryobiology ◽  
1998 ◽  
Vol 36 (1) ◽  
pp. 61-70 ◽  
Author(s):  
P. Dutkowski ◽  
S. Schönfeld ◽  
B. Odermatt ◽  
T. Heinrich ◽  
T. Junginger

1999 ◽  
Vol 31 (6) ◽  
pp. 2437-2438 ◽  
Author(s):  
P Cascales ◽  
V Fernández-Cornejo ◽  
F Sanchez-Del Campo ◽  
M de Torre ◽  
M.R Sanchez-Eixeres ◽  
...  

1992 ◽  
Vol 5 ◽  
pp. S329-S335 ◽  
Author(s):  
W. Gao ◽  
R. J. Currin ◽  
J. J. Lemasters ◽  
H. D. Connor ◽  
R. P. Mason ◽  
...  

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.


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