An Ultrstructural Study on the Acute Hepatic Necrosis Induced by Endotoxin |
내독소투여로 인한 급성 간괴사의 초미형태학적 연구 |
서인수; 정재홍; 김정희 |
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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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