|
Shock , gastrointestinal bleeding , and liver transplantation is often inevitable lead to liver ischemia , blood flow through the liver metabolic dysfunction and structural damage exacerbated this phenomenon is to hepatic ischemia-reperfusion (ischemia reperfusion, IR) injury . IR is widespread pathophysiological process , therefore exploring the mechanism of injury , and to find ways to protect the ischemic liver cells is an urgent need to resolve the issue . Liver IR injury is more than one factor in a complex process , that the basic mechanism of IR injury , oxygen free radicals (oxygen free radical, OFR) generation increased and the role of intracellular calcium overload , at the same time the inflammatory response of neutrophils infiltration , the microcirculation also with close to IR injury . Heme oxygenase (heme oxygenase, HO) are mainly distributed in the lungs , liver , spleen , and reticuloendothelial system , the rate-limiting enzyme of heme metabolism , decomposition of heme to form the same amount of carbon monoxide (carbon monoxide, CO) and bile chlorophyll and the release of iron atoms . HO and its metabolites through antioxidant , anti-inflammatory , maintain microcirculation role against IR injury . Intracellular calcium overload is a common pathway of cell irreversible damage . Under physiological conditions , the intracellular the of Ca 2 concentration mainly depends cell membrane of of Ca 2 < / sup > -ATPase Ca 2 transport regulation . Neutrophils are one of the important cellular components involved in the process of IR injury . Intercellular adhesion molecule (intercellular adhesion molecule-1, ICAM-1) is mediated neutrophil and endothelial cell adhesion adhesion molecule , plays an important role in reperfusion injury .
|