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زیست شناسی::
هپاتوسیت
The second line of defense, discussed below, is a population of hepatic progenitor cells that are normally quiescent but that are activated when the injury is severe and adult hepatocytes cannot regenerate well due to senescence, alcohol abuse, or disease.
These lipopolysaccha- rides activate some non-hepatocytes to secrete paracrine factors that allow the remaining hepatocytes to re-enter the cell cycle.
Hepatocytes that are still connected to one another in an epithelium cannot respond to HGF, however.
Hepatocytes activate cMet (the receptor for HGF) within an hour of partial hepatecto- my, and the blocking of cMet (by RNA interference or knockout) blocks liver regeneration (Borowiak et al. 2004; Huh et al. 2004
;The trauma of partial hepatectomy may activate metalloproteinases that digest the extracellular matrix and permit the hepatocytes to separate and proliferate.
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عمومی::
هپاتوسیت
Multiple factors contribute to postoperative liver failure, but the basic physiology is driven by ischemia of the hepatocytes.
Hypotension secondary to hypovolemia, hemorrhage, and vaso- dilation all result in a decreased MAP, which diminishes nutritive hepatic artery and portal vein flow. ftis mechanism is also involved in some cases of liver failure observed after general anes- thesia or laparoscopic procedures in which hepatocyte hypoperfu- sion may not be as readily evident.
Because the cirrhotic liver already has significantly reduced numbers of hepatocytes, the ischemic injury to the remaining hepatocytes is manifested in decreased synthetic function with insufficient generation of criti- cal proteins such as clotting factors and albumin.
In addition, the decrease in hepatocytes limits the ability of the liver to perform normal metabolic functions, and toxins such as ammonia and drug metabolites may build up.
, bleeding, encephalopathy, ascites) are in some way attributable to hepatocyte death.
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