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Hepatic ischemia-reperfusion injury in the pathogenesis and prevention of
PAGE \* MERGEFORMAT 18
Hepatic ischemia-reperfusion injury in the pathogenesis and prevention of
Ischemia-reperfusion injury was first proposed by in 1960 Jennings was referring to tissues and organs after ischemia and reperfusion, not only can not make tissues and organs function recovery, but increased tissue and organ dysfunction and structural damage. Ischemia-reperfusion injury in a number of vital organs including the heart, liver, lung, kidney, gastrointestinal tract, etc. can occur. Hepatic ischemia-reperfusion injury (HIRI) is common in liver surgery the pathological process, common in shock and need to block the blood flow in hepatic liver surgery and liver transplantation and other pathophysiological process. The pathophysiologic mechanism of its occurrence complicated, there are many factors involved, the formation of mutual restraint and mutually reinforcing relationship. Including inflammatory cell infiltration and platelet aggregation, reactive oxygen intermediates (ROI) generation and release of various inflammatory mediators (such as adhesion molecules and leukotrienes) and vasoactive matter (like a produce such as nitric oxide and endothelin-related ) [1].
A hepatic ischemia - reperfusion injury in the mechanism
A reactive oxygen intermediates (ROI) of the production and release:
With the large accumulation of liver hypoxia ATP metabolites hypoxanthine and oxygen react. Generate ROI (high activity, such as peroxide and hydroxyl goods). As the ROI in structure to the orbit away from it does not match one or more electronic features, thereby ROI with high activity and potential toxicity. The liver ROI generated during ischemia and hypoxia can damage cells through several mechanisms: ① to selectively damage neighboring molecules such as lipids, proteins and nucleic acids; ② increase in the signal transmission of neutrophil chemotaxis and the resulting is activated; ③ NO reaction with the highly toxic peroxides [2]. A lar
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