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Original Articles
- An Immunohistochemical Study on the Distribution of Endotoxin.
- Tae In Park, Jung Ja Park, Jyung Sik Kwak, In Soo Suh
- Korean J Pathol. 1994;28(3):260-271.
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Abstract
- This study was performed to investigate the distribution of endotoxin in various organs after intraperitoneal injection of E. coli homogenator(0111:B4, 3X10(9)cells/200g of body weight). Sprague-Dawley rats were intraperitoneally injected with E. coli homogenator and sacrificed 1 and 3 hours after injection. The lung, liver, and kidney were immunohistochemically stained with avidin-biotin complex method and observed by light and electron microscopy. On the light microscopy, granular deposits of reaction products of immunohistochemical stain were found on the cytoplasmic membrane of endothelial cells and some of parenchymal cells of all organs observed. Electron microscopic study revealed finely granular reaction products on the surface of endothelial cells and some of parenchymal cells. The pinocytotic vesicles of endothelial cells demonstrated reaction products in the early phase of experiment. The distribution of reaction products were prominent in the liver among three organs. The Kupffer cells showed the most sensitive and strongest positive reaction. The hepatocytes and endothelial cells revealed weak positive reaction 3 hours later. The alveolar macrophages of the lung were also positive from the early phase of endotoxemia, while the pneumocytes and alveolar septa demonstrated weakly positive reaction in the later phase. The capillary endothelium of the kidney revealed positive reaction from the early phase. According to above results, it is concluded that the endotoxin entered into the systemic circulation was captured in the liver and lung. And both mononuclear phagocytic system and endothelial cells could be activated or damaged by endotoxin.
- The effects of Broad Spectrum Antibiotics and Endotoxin to the Carbon Tetrachloride-induced Liver Injury.
- Hyun Ho Shin, O Joon Kwon, Yoon Kyung Sohn, In Soo Suh, Tae Joong Sohn
- Korean J Pathol. 1992;26(4):329-337.
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Abstract
PDF - This study was performed to investigate the effect of endotoxin to the CCl4-induced liver injury. Twelve Sprague-Dawley rats were intraperitoneally injected 1.6 g/kg CCl4 as control group. Another 24 rats were orally administrated 300 mg/kg of neomycin at 16 and 3 hours prior to CCl4 injection as experimental group. Twelve among them were intraperitoneally infected 1.0 mg/kg of endotoxin(E-Coli, 0111:B4, No L-2630, lipopolysaccharide, Sigma, USA) and CCl4 simultaneously for offsetting neomycin effect. The rats were sacrificed at 1, 4, 10, and 24 hours after CCl4 injection. The liver tissues from all experimental groups were observed by light and electron microscopy. The results obtained were summarized as follows: In the CCl4 only group, the hepatocytes revealed sweling of ER and mitochondria with many lipid droplet in the cytoplasm. Focal cellular necrosis was seen at the later phase. The Kupffer cells were activated and showed many cytoplasmic processes, secondary lysosomes, and vaculoles. The endothelial cells were edematous. Several neutrophils, platelets, and microthrombi were scattered in the sinusoid. In the neomycin-CCl4-endotoxin administrated group, both hepatocytic destruction and intrasinusoidal microthrombi formation were more pronounced. In the neomycin pretreated group, the hepatocytes revealed mild cellular destruction without necrosis. There is no intrasinusoidal microthrombi. According to these results, it would be concluded that the small dosage of gastrointestinal tract-derived endotoxin affects to the liver injury caused by CCl4. The synergistic effects of CCl4 and gastrointestinal tract-derived endotoxin which can not be detoxified by damaged Kupffer cells, may be more important in the pathogenesis of CCl4-induced liver injury.
- A Study on the Pathogenesis of Renal Papillary Necrosis Induced by Endotoxin.
- Kyung Rak Sohn, Tae Joong Sohn
- Korean J Pathol. 1989;23(4):416-454.
- 1,594 View
- 20 Download
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Abstract
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- The author carried out an experimentation to clarify a possible pathogenesis of renal papillary necrosis induced by an univisceral Shwartzman reaction. The experimental animals were healthy white rabbits in weighing between 1.7 kg and 3.0 kg. Under the condition of ureterostomy, animals were pretreated with 0.5 cc of 50% ethyl alcohol and followed by administration of 0.2 ~ 1.5 mg endotoxin (E. coli 026 : B6, bacto lipopolysaccharide B. Difco, U.S.A.) as preparation in the renal pelvis. And then sacrificed at 10 minutes, 30 minutes, 1 hour, 2 hours, 6 hours and 24 hours after intravenous injection of 0.2 mg or 0.6 mg endotoxin through the ear veins, subjection to examine light and electron microscopically. The obtained results were summarized as follows: Papillary necrosis was developed in 88% among 18 cases excluding 6 cases died before sacrification. There were two types of necrosis, namely papillary and medullary type, but the former and combined forms of both types were the most common findings. Initial main target site of injury in renal papilla induced by endotoxiin was the endothelium of vasa recta and then followed by the Henle's loop, interstitial cell and collecting tubule respectively. Vascular injuries such as swelling and detachment of endothelium were observed since 10 minutes after endotoxin injection. Henle's loop showed stratification of basement membrane without consistent features with time lapses and initially observed fatty vaculoes at 1 hour after endotoxin injection were more eminent in 24 hours group. Main changes of interstitial cells were decrease of lipid droplets while increase of fatty vacuoles; the latter were initially observed in 1 hour group and more eminent in 24 hours group. Collecting tubule showed many fatty vacuoles especially in 24 hours group. It is thought that emergence of fatty vacuoles seems to be a kind of immature lipid droplets to compensate the increased demand of PC release due to continuous ischemic condition. In conclusion, it is thought that ischemic injury due to the vascular changes is pathogenic mechanism producing renal papillary necrosis. Endotoxin induced univisceral Shwartzman reaction in the kidney may be a good experimental model in studying renal papillary necrosis.
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