[The study of the mechanism of hepatocyte injury during endotoxin (ET) shock--special reference with a role of polymorphonuclear neutrophils (PMN)].
The present study was designed to indicate the role of ET-activated PMN on hepatocyte injury during ET shock. In this study ET shock was made by intravenous administration of 5mg/kg ET to rats. PMN and plasma were sequentially collected from rats before and 6, 12, 24 hours after administration of ET. Hepatocytes were collected from rats without administration of ET. Plasma glutamate dehydrogenase, peripheral PMN counts and superoxide production of PMN were higher at 12 hours than the value of before and at 6, 24 hours. Cell damages and the infiltration of PMN into the liver were most remarkable at 12 hours. Phagocytosis of PMN was lower only at 6 hours than the value of before. In vitro, the hepatocyte cytotoxicity of PMN reached a peak at 12 hours, but was not found at 24 hours. The findings suggested that the microcirculatory insufficiency and ET-activated PMN played important roles of hepatocyte injury during ET shock.
Ishikawa
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First Department of Surgery, Nippon Medical School, Tokyo, Japan.
D000818:Animals; D002478:Cells, Cultured; D005969:Glutamate Dehydrogenase / Q000097:blood; D008099:Liver / Q000098:blood supply / Q000166:cytology / Q000473:pathology*; D008297:Male; D008833:Microcirculation; D009504:Neutrophils / Q000378:metabolism / Q000502:physiology*; D010587:Phagocytosis; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012772:Shock, Septic / Q000473:pathology*; D013997:Time Factors
D017382:Reactive Oxygen Species; D005969:Glutamate Dehydrogenase