Fine structure and detoxification kinetics in kupffer cells after injection of endotoxin in rats.
10.12701/yujm.1993.10.2.313
- Author:
Joon Hyuk CHOI
;
Won Hee CHOI
;
Tae Sook LEE
- Publication Type:Original Article
- MeSH:
Animals;
Endoplasmic Reticulum, Rough;
Endoplasmic Reticulum, Smooth;
Endotoxemia;
Estrogens, Conjugated (USP);
Euchromatin;
Fibrin;
Glycogen;
Golgi Apparatus;
Hepatocytes;
Hypertrophy;
Ischemia;
Kinetics*;
Kupffer Cells*;
Liver;
Lysosomes;
Microscopy, Electron;
Mitochondria;
Necrosis;
Neutrophils;
Pinocytosis;
Rats*;
Vacuoles
- From:Yeungnam University Journal of Medicine
1993;10(2):313-337
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The aim of this study was to clarify the role of Kupffer cells in the mechanism of endotoxin-induced liver injury. The study on fine structure of Kupffer cells was performed after the injection of endotoxin. The endotoxin(Escherichia soli lipopolysaccharide 026: B6, 1.5mg/100 g of body weight) was intraperitoneally injected in Sprague-Dewley rats. Animals were sacrificed at 1/4, 1/2, 1, 2, 4, 8, 16, 24, 72 and 120 hours after the injection of endotoxin. Livers were extirpated and processed to be examined by light and electron microscopy. The results obtained were summerized as follows: Early changes observed in liver after endotoxin injection included the increased number and hypertrophy of Kupffer cells, infiltration of neutrophils and presence of fibrin thrombi within the sinusoids. The coritinuous increase of the Kupffer cells in number with hypertrophy, congestion and infiltration of inflammatory cells within the sinusoids were observed. Hepatocytes showed* fatty change and occasional necrosis. At 72 hours the congestion decreased. At 120 hours the number of Kupffer cells was increased, but the morphology of Kupffer cells became similar to that of the control group. The numbers and sizes of primary and secondary lysosomes and amount of euchromatin of Kupffer cells increased. Swellings and increase in number of mitochondria, Golgi complex, smooth endoplasmic reticulum, rough endoplasmic reticulum were evident. Microthrombi were present within the sinusoids. The swelling of rough endoplasmic reticulum and mitochondria, decrease of glycogen particles, fatty change, hypoxic vacuoles, pyknotic nuclei and occasional necrosis were observed in hepatocytes. At 72 hours the number of secondary lysosomes in Kupffer cells decreased. At 120 hours the morphology of Kupffer cells became similar to that of the control group. According to these results, it was postulated that the endotoxin was initially taken up by pinocytosis into Kupffer cells and degraded in secondary lysosomes of activated Kupffer cells. Kupffer cells may play an important role in the defense mechanism of liver during endotoxemia. The dysfunction of Kupffer cells and ischemia by sinusoidal microthrombi may cause liver injury.
