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Keimyung Medical Journal 1987;6(2):177-202.
An Ultrstructural Study on the Acute Hepatic Necrosis Induced by Endotoxin
내독소투여로 인한 급성 간괴사의 초미형태학적 연구
서인수; 정재홍; 김정희
Abstract
The author has carried out an ultrastructural study on the morphological changes in the rat liver induced by endotoxin to clarify the disease process and mechanisms involved of endotoxin-induced hepatocellular injury and the reactions of Kupffer cells to the administered endotoxin. The experimental animals were divided into two groups: the first group; animals were given endotoxin through tail vein(a) and another group; through portal vein(b). Animals were sacrificed 30 minutes; 1;2;4;8; and 24 hours after injections of endotoxin. Livers were extirpated and examined by light and electron microscopy. The results obtained were summarized as follows: The tail vein group(a) revealed sinusoidal microthrombi; endothelial detachment; widening and hemorrhages of Disse space together an infiltration of polymorphonuclear leukocytes; in early phase of hepatocellular injury. Destruction of Kupffer cells; imbibition of sinusoidal material into the hepatocytes; and hepatocytic necrosis were observed 2 hours after endotoxin administration. The portal vein group(b) showed increased phagocytic activity of Kupffer cells; however; no hepatic necrosis nor microthrombi formation. It can be concluded; therefore: That judging from the results of experimental study; the Kupffer cells react to the endotoxin reached to the liver by the functions of phagocytosis; clearance; and inactivation of endotoxin through the release of intracytoplasmic lysosomal enzymes and opsonin-like material. The disease processes and mechanisms involved of hepatocellular injury found in the endotoxemia state may be stated that firstly; difficulty in clearing and removing of the endotoxin from the liver due to impaired peripheral circulation; secondly; ischemia of hepatic cells brought about by the generalized dissemimated intravascular coagulation; thirdly; loss of Kupffer cell function to detoxify the endotoxin rendered by the loss of energy to reduced circulation.
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