Linked Life Data

12859717

Source:http://linkedlifedata.com/resource/pubmed/id/12859717

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-7-15
pubmed:abstractText
This review highlights recent advances in our understanding of mechanisms underlying reperfusion injury to the liver after warm hepatic ischemia. Sinusoidal endothelial cells and hepatocytes are targets of injury in the early 'cytotoxic' phase, although participation of apoptosis in the cell-death process remains contentious. Kupffer cells may play an important role as the initial cytotoxic cell type and are likely a source of reactive oxygen species and proinflammatory mediators, particularly tumor necrosis factor (TNF)-alpha. The latter are involved with subsequent neutrophil activation and recruitment. Microcirculatory disruption results from an imbalance between the actions of vasoconstrictors and vasodilators, such as nitric oxide, and also has a major impact on reperfusion injury. There is growing evidence that a brief prior ischemia-reperfusion period, termed 'ischemic preconditioning', is hepatoprotective. This can be mimicked by drugs that produce oxidative stress, and by interleukin-6 and TNF-alpha; both these cytokines are involved with priming hepatocytes to enter the cell cycle. Several mechanisms have been implicated including mobilization of adenosine and activation of adenosine type 2 receptors, nitric oxide, abrogation of TNF synthesis, preservation of energy metabolism, protection of the microcirculation and accelerated cell-cycle entry. A better understanding of preconditioning mechanisms will lead to novel approaches to improve outcomes of liver surgery.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0815-9319
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
891-902
pubmed:meshHeading
pubmed-meshheading:12859717-Adenosine, pubmed-meshheading:12859717-Animals, pubmed-meshheading:12859717-Apoptosis, pubmed-meshheading:12859717-Cell Adhesion Molecules, pubmed-meshheading:12859717-Hepatocytes, pubmed-meshheading:12859717-Humans, pubmed-meshheading:12859717-Hydrogen-Ion Concentration, pubmed-meshheading:12859717-Interleukin-1, pubmed-meshheading:12859717-Interleukin-6, pubmed-meshheading:12859717-Ischemic Preconditioning, pubmed-meshheading:12859717-Kupffer Cells, pubmed-meshheading:12859717-Liver, pubmed-meshheading:12859717-Liver Circulation, pubmed-meshheading:12859717-Microcirculation, pubmed-meshheading:12859717-Nitric Oxide, pubmed-meshheading:12859717-Reactive Oxygen Species, pubmed-meshheading:12859717-Reperfusion Injury, pubmed-meshheading:12859717-Tumor Necrosis Factor-alpha, pubmed-meshheading:12859717-Warm Ischemia
pubmed:year
2003
pubmed:articleTitle
Hepatic ischemia reperfusion injury: pathogenic mechanisms and basis for hepatoprotection.
pubmed:affiliation
Storr Liver Unit, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Westmead, New South Wales, Australia.
pubmed:publicationType
Journal Article, Review