INVOLVEMENT OF THROMBOXANE A2-THROMBOXANE A2 RECEPTOR SYSTEM OF THE HEPATIC SINUSOID IN PATHOGENESIS OF COLD PRESERVATION/REPERFUSION INJURY IN THE RAT LIVER GRAFT

1995 ◽  
Vol 59 (7) ◽  
pp. 957-961 ◽  
Author(s):  
Satoshi Ishiguro ◽  
Shigeki Arii ◽  
Kazunobu Monden ◽  
Shin-ichi Fujita ◽  
Toshio Nakamura ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Thromboxane A2 ◽  
Liver Graft ◽  
Receptor System ◽  
Cold Preservation ◽  
Thromboxane A2 Receptor ◽  
Hepatic Sinusoid

scholarly journals Heavy Water (D2O) Containing Preservation Solution Reduces Hepatic Cold Preservation and Reperfusion Injury in an Isolated Perfused Rat Liver (IPRL) Model

2019 ◽  
Vol 8 (11) ◽  
pp. 1818
Author(s):  
Shingo Shimada ◽  
Moto Fukai ◽  
Kengo Shibata ◽  
Sodai Sakamoto ◽  
Kenji Wakayama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Rat Liver ◽  
Heavy Water ◽  
Biological Effects ◽  
Energy Charge ◽  
Liver Graft ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Cold Preservation

Background: Heavy water (D2O) has many biological effects due to the isotope effect of deuterium. We previously reported the efficacy of D2O containing solution (Dsol) in the cold preservation of rat hearts. Here, we evaluated whether Dsol reduced hepatic cold preservation and reperfusion injury. Methods: Rat livers were subjected to 48-hour cold storage in University of Wisconsin (UW) solution or Dsol, and subsequently reperfused on an isolated perfused rat liver. Graft function, injury, perfusion kinetics, oxidative stress, and cytoskeletal integrity were assessed. Results: In the UW group, severe ischemia and reperfusion injury (IRI) was shown by histopathology, higher liver enzymes leakage, portal resistance, and apoptotic index, oxygen consumption, less bile production, energy charge, and reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio (versus control). The Dsol group showed that these injuries were significantly ameliorated (versus the UW group). Furthermore, cytoskeletal derangement was progressed in the UW group, as shown by less degradation of α-Fodrin and by the inactivation of the actin depolymerization pathway, whereas these changes were significantly suppressed in the Dsol group. Conclusion: Dsol reduced hepatic IRI after extended cold preservation and subsequent reperfusion. The protection was primarily due to the maintenance of mitochondrial function, cytoskeletal integrity, leading to limiting oxidative stress, apoptosis, and necrosis pathways.

Carrier-Mediated Active Transport of a Novel Thromboxane A2 Receptor Antagonist [2-(4-Chlorophenylsulfonylaminomethyl)indan-5-yl]acetate (Z-335) into Rat Liver

2002 ◽  
Vol 30 (5) ◽  
pp. 498-504 ◽  
Author(s):  
Yoshihiro Kawabata ◽  
Shigeru Furuta ◽  
Yutaka Shinozaki ◽  
Tadashi Kurimoto ◽  
Ryuichiro Nishigaki
Keyword(s):  
Receptor Antagonist ◽  
Active Transport ◽  
Rat Liver ◽  
Thromboxane A2 ◽  
Thromboxane A2 Receptor

Role of the Thromboxane A2 Receptor in the Vasoactive Response to Ischemia-Reperfusion Injury

1999 ◽  
Vol 104 (5) ◽  
pp. 1393-1396 ◽  
Author(s):  
Peter J. Mazolewski ◽  
Allen C. Roth ◽  
Hans Suchy ◽  
Linda L. Stephenson ◽  
William A. Zamboni ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Thromboxane A2 ◽  
Thromboxane A2 Receptor

Cyclosporine overcomes cold preservation/reperfusion injury of liver graft: Chemokine release and liver ultrastructure

1997 ◽  
Vol 4 (4) ◽  
pp. 423-430 ◽  
Author(s):  
Tetsuji Kai ◽  
Yang Il Kim ◽  
Hirokazu Kitamura ◽  
Katsunori Kawano ◽  
Seigo Kitano
Keyword(s):  
Reperfusion Injury ◽  
Liver Graft ◽  
Cold Preservation ◽  
Liver Ultrastructure

Hydrogen Gas Ameliorates Hepatic Reperfusion Injury After Prolonged Cold Preservation in Isolated Perfused Rat Liver

2016 ◽  
Vol 40 (12) ◽  
pp. 1128-1136 ◽  
Author(s):  
Shingo Shimada ◽  
Kenji Wakayama ◽  
Moto Fukai ◽  
Tsuyoshi Shimamura ◽  
Takahisa Ishikawa ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Liver ◽  
Hydrogen Gas ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Cold Preservation

scholarly journals The Hepatoprotective Effect of Sodium Nitrite on Cold Ischemia-Reperfusion Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Li ◽  
Zihui Meng ◽  
Yuliang Liu ◽  
Rakesh P. Patel ◽  
John D. Lang
Keyword(s):  
Reperfusion Injury ◽  
Sodium Nitrite ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Combined Treatment ◽  
Solid Organ Transplantation ◽  
Liver Graft ◽  
Solid Organ ◽  
Post Transplantation ◽  
Cold Preservation

Liver ischemia-reperfusion injury is a major cause of primary graft non-function or initial function failure post-transplantation. In this study, we examined the effects of sodium nitrite supplementation on liver IRI in either Lactated Ringer's (LR) solution or University of Wisconsin (UW) solution. The syngeneic recipients of liver grafts were also treated with or without nitrite by intra-peritoneal injection. Liver AST and LDH release were significantly reduced in both nitrite-supplemented LR and UW preservation solutions compared to their controls. The protective effect of nitrite was more efficacious with longer cold preservation times. Liver histological examination demonstrated better preserved morphology and architecture with nitrite treatment. Hepatocellular apoptosis was significantly reduced in the nitrite-treated livers compared their controls. Moreover, liver grafts with extended cold preservation time of 12 to 24 hours demonstrated improved liver tissue histology and function post-reperfusion with either the nitrite-supplemented preservation solution or in nitrite-treated recipients. Interestingly, combined treatment of both the liver graft and recipient did not confer protection. Thus, nitrite treatment affords significant protection from cold ischemic and reperfusion injury to donor livers and improves liver graft acute function post-transplantation. The results from this study further support the potential for nitrite therapy to mitigate ischemia-reperfusion injury in solid organ transplantation.

Sign in / Sign up

Export Citation Format

Share Document