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Review
. 2012:2012:298657.
doi: 10.1155/2012/298657. Epub 2012 May 9.

The current state of knowledge of hepatic ischemia-reperfusion injury based on its study in experimental models

M Mendes-Braz  1 , M Elias-Miró, M B Jiménez-Castro, A Casillas-Ramírez, F S Ramalho, C Peralta
Affiliations
Review

The current state of knowledge of hepatic ischemia-reperfusion injury based on its study in experimental models

M Mendes-Braz et al. J Biomed Biotechnol. 2012.

Abstract

The present review focuses on the numerous experimental models used to study the complexity of hepatic ischemia/reperfusion (I/R) injury. Although experimental models of hepatic I/R injury represent a compromise between the clinical reality and experimental simplification, the clinical transfer of experimental results is problematic because of anatomical and physiological differences and the inevitable simplification of experimental work. In this review, the strengths and limitations of the various models of hepatic I/R are discussed. Several strategies to protect the liver from I/R injury have been developed in animal models and, some of these, might find their way into clinical practice. We also attempt to highlight the fact that the mechanisms responsible for hepatic I/R injury depend on the experimental model used, and therefore the therapeutic strategies also differ according to the model used. Thus, the choice of model must therefore be adapted to the clinical question being answered.

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Figures

Figure 1
Figure 1
Mechanisms involved in hepatic ischemia-reperfusion injury. EC, endothelial cell; ET, endothelin; UPR/ER, unfolded protein response/endoplasmic reticulum; IRE1, inositol-requiring enzyme 1; PERK, PKR-like ER kinase; SLP, secretory leukocyte protease inhibitor; ICAM, intracellular cell adhesion molecule; VCAM, vascular cell adhesion molecule; GM-CSF, granulocyte-macrophage colony-stimulating factor; IL, interleukin; INF, interferon; TNF, tumor necrosis factor; PAF, platelet-activating factor; LTB4, leucotriene B4; KC, Kupffer cell; X/XOD, xanthine/xanthine oxidase; Cyt c: cytochrome c.
Figure 2
Figure 2
Models of global normothermic liver ischemia. (a) Pringle maneuver. (b) Splecnocaval shunt. (c) Portojugular shunt. (d) Spleen transposition.
Figure 3
Figure 3
(a) Transposition of the spleen to the subcutaneous tissue in the left hypochondrium. (b) Abdominal cavity after three weeks of the transposition of the spleen. (c) Anhepatic phase in recipient with SPS. No intestinal congestion is observed secondary to clamping of different vessels. (d) Anhepatic phase in recipient without SPS. Intestinal congestion is observed secondary to clamping of the different vessels.
Figure 4
Figure 4
Liver transplantation procedure. (a) Suprahepatic cava vein prepared for the anastomosis. (b) Inferior vein cava cuff attachment. (c) Anhepatic phase in the recipient rat. (d) Anastomosis of suprahepatic cava vein by continuous suture. (e) Portal vein anastomosis through the cuff method. (f) Anastomosis of the bile duct.
Figure 5
Figure 5
Illustrative representation of machine reperfusion.
See this image and copyright information in PMC

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