Hepatic ischemia-reperfusion injury

Background: The morbidity associated with liver transplantation and major hepatic resections is partly a result of ischemia-reperfusion injury. Data Sources: The entire world literature on the subject was searched via Medline. Keywords included reperfusion injury, transplantation, liver resection, n...

Full description

Saved in:
Bibliographic Details
Published in:The American Journal of Surgery 2001-02, Vol.181 (2), p.160-166
Main Authors: Serracino-Inglott, Ferdinand, Habib, Nagy A, Mathie, Robert T
Format: Article
Language:English
Subjects:
Adenosine - physiology
Animal models
Antioxidants
Biological and medical sciences
Chemical synthesis
Chemokines
Cytokines
Cytokines - physiology
Endothelins
Endothelins - physiology
Free radicals
Gastroenterology. Liver. Pancreas. Abdomen
Hepatectomy
Hepatic resection
Hepatic transplantation
Humans
Hypotension
Inflammation
Injuries
Ischemia
Ischemic preconditioning
Kupffer Cells
Leukocytes
Leukocytes (neutrophilic)
Liver
Liver - blood supply
Liver Transplantation
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Morbidity
Neutrophils
NF-kappa B - physiology
Nitric oxide
Nitric Oxide - physiology
Nuclear factor-κB
Other diseases. Semiology
Pathophysiology
Plasma
Preconditioning
Reperfusion
Reperfusion Injury
Transplantation
Tumor necrosis factor-TNF
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background: The morbidity associated with liver transplantation and major hepatic resections is partly a result of ischemia-reperfusion injury. Data Sources: The entire world literature on the subject was searched via Medline. Keywords included reperfusion injury, transplantation, liver resection, nitric oxide, endothelin, cytokines, Kupffer cells, ischemic/ischaemic preconditioning, and nuclear factor-κB. Conclusions: An imbalance between endothelin and nitric oxide levels results in failure of the hepatic microcirculation at the onset of reperfusion. Activation of nuclear factor-κB in the liver promotes proinflammatory cytokine and adhesion molecule synthesis. These result in oxygen-derived free radical production and neutrophil recruitment, further contributing to cellular injury. Various therapeutic modalities acting on the above mediators have been successfully used to attenuate reperfusion injury in animal models of hepatic transplantation and resection. Application of the knowledge gained from animal models of hepatic ischemia-reperfusion to the clinical setting will improve the outcome of hepatic surgery.
ISSN:0002-9610
1879-1883
DOI:10.1016/S0002-9610(00)00573-0