Journal of Pathology and Translational Medicine

Original Articles

Experimental Study on Shark Liver Oil-Induced Lipoid Pneumonia in Rats.: Mee Soo Chang, Eui Keun Ham; Korean J Pathol. 1997;31(8):711-722.

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Abstract PDF: The purpose of this experiment is to evaluate the histopathologic findings of shark liver oil-induced lipoid pneumonia, and to determine whether shark liver oil is absorbed through lymphatics and the venous system or not. A single intratracheal administration of shark liver oil (0.6 ml/kg of B.W.) was given to Sprague-Dawley rats. They were then sacrificed sequentially from 1 hour to 12 weeks after injection. We investigated the chest radiographic findings, the serum total lipid concentration of blood obtained by cardiac puncture, lipid-laden alveolar macrophage index of the bronchoalveolar lavage fluid, and the histopathology of tracheobronchial lymph nodes and the lung (Oil red O stain & H&E stain). Chest radiographs showed no specific findings; ill-defined hazy, linear, small patch radioopacity, air space consolidation or collapse. Thirty-six percent of the experimental rats revealed normal findings. Within the lung, the shark liver oil appeared either as highly emulsified fine granules in the cytoplasm of the alveolar macrophage or as free, round oil masses. The area of the lung accumulated with lipid material was maximized 1 week after injection, and then decreased thereafter. The tissue reactions were cuboidal metaplasia of the alveolar lining, widening and lymphocytic infiltration of the alveolar septa and granuloma formation (3% of experimental rats) as a reaction to a foreign body. There were also lung abscesses due to superimposed bacterial infection (5% of experimental rats). With time after the injection of the oil, the serum total lipid tended to increase and the intracellular lipid of the alveolar macrophages in the bronchoalveolar lavage fluid tended to decrease. In summary, the histopathologic findings of the lung in the experimental lipoid pneumonia were interstitial chronic inflammation and granulomas with the presence of lipoid material in the lung parenchyma, and shark liver oil appeared to be absorbed in the blood and the lymph, then metabolized.

Effect of Atorvastatin, a HMG-CoA Reductase Inhibitor, in Experimental Colitis in Mice.: Hyo Jin Park, Tae Woon Kim, Jae Nam Seo, Kwon Ik Oh, Eun Young Choi, Hyung Sik Shin, Young Euy Park; Korean J Pathol. 2004;38(6):401-407.

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Abstract PDF: BACKGROUND
The statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are approved for cholesterol reduction, and may also be beneficial in the treatment of inflammatory disease. In this study, atorvastatin was tested in experimental colitis, a disease model of inflammatory bowel disease.
METHODS
To induce colitis, dextran sodium sulfate (DSS) or trinitrobenzene sulfonic acid (TNBS) were administrated to C57BL/6 or BALB/c mice. Mice were monitored daily for loss of body weight and survival for indicated days. Colon length and histology were examined after sacrifice.
RESULTS
The administration of DSS induced marked colonic inflammation and shortening, and resulted in a loss of body weight. DSSinduced colitis was not affected by atorvastatin treatment, but in contrast, the administration of atorvastatin relieved TNBS-induced colitis with a resultant rapid recovery of weight loss and a reduction in colonic length shortening. Histologically, inflammatory cell infiltration in the colonic wall, mucosal ulceration and crypt disruption were also suppressed in atorvastatin treated mice.
CONCLUSION
These results suggest that atorvastatin preserves intestinal integrity in colitis, probably via the modulation of Th cell-mediated immune response, in a manner independent of innate immunity.

Study on Histopathologic Changes of Suckling Rats Inoculated with Hantaan Virus.: Hye Je Cho, Luck Ju Paek, Ho Wang Lee, Eui Keun Ham; Korean J Pathol. 1991;25(3):223-237.

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Abstract PDF: Hantaan and related viruses have been implicated as causative agents for a diverse group of human diseases known collectively as "hemorrhagic fevers with renal syndrome" (HFRS). Outbred SD rats obtained within 24 hours after birth were inoculated by intracerebral (the first group) or intramuscular routes (the second group) with 10(9.5)/ml DL50 of Hantaan seed virus suspension in 0.02 ml and 0.1 ml, respectively. Brain, lung, liver, kidney and spleen were used for virus antigen detection by immunofluorecence and histopathologic examination. In the first group, immunofluorescent intensity of virus antigen was increased in all organs (especially brain) and persisted until time of death(day 9). The histopathologic changes were relatively mild in brain and spleen and unremarkable in liver, lung and kidney. In the second group, immunofluorescent intensity of virus antigen was markedly increased in brain until time of death(day 17), but decreased in other organs. The histopathologic findings, such as meningoencephalitis, interstitial pneumonitis with focal hemorrhage, and lymphoid hyperplasia of splenic white pulp were much prominent compared to the first group. However, those of liver and kidney were unremarkable. The chronology of virologic and pathologic findings in Hantaan-infected suckling rats suggests a possible immune-mediated mechanism in disease pathogenesis.

An Experimental Study of Vibrio vulnificus Infection in Mice.: Moon Ho Yang; Korean J Pathol. 1991;25(2):123-146.

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Abstract PDF: An experimental of Vibrio vulnificus infection has been performed with the intravenous, subcutaneous and oral inoculation of Vibrio vulnificus into ICR mice. The results are as follows: 1) The LD50 of the intravenous, subcutaneous and oral inoculation of Vibrio vulnificus were 1.6x10(7) cells/ml, 4.0x10(7) cells/ml, and 2.5x10(9) cells/ml, respectively. 2) In the experimental group without treatment with CC14, the survival rates for intravenous inoculation were 100% (1/2 LD50), 39.1% (LD50), and 8.3% (2 LD50). The survival rates for subcutaneous inoculation groups were 100% (1/2 LD50), 46.9% (LD50), and 18.8% (2 LD50). And the survival rates for oral inoculation groups were 100% (1/2 LD50), 53.1% (LD50), and 43.8% (2 LD50). 3) In those treated with CC14 0.05 ml, the survival rates for intravenous inoculation groups were 43.8% (1/2 LD50), 29.1% (LD50), 0% (2 LD50). The survival rates for subcutaneous inoculation groups were 59.4% (1/2 LD50), 40.6% (LD50), and 9.4% (2 LD50). The survival rates for oral inoculation groups were 68.8% (1/2 LD50), 46.9% (LD50), and 18.8% (2 LD50). In those treated with CC14 0.1 ml, the survival rates for intravenous inoculation groups were 25.0% (1/2 LD50), 10.4% (LD50), and 0% (2 LD50). The survival rates for subcutaneous inoculation groups were 43.8% (1/2 LD50), 21.9% (LD50), 0% (2 LD50). The survival rates for oral inoculation groups were 50.0% (1/2 LD50), 37.5% (LD50), and 0% (2 LD50). 4) Liver, lungs, meninges and brain, kidneys, heart, gastrointestinal tract and spleen showed septic inflammatory findings. Their degree of inflammation were different according to the severity of hepatic damage and the inoculum size.

An Experimental Study of Pathogenesis of Duodenal Ulceration Produced by Mepirizole.: Myung Jae Kang, Jae Ryong Jung, Hye Soo Lee, Sang Ho Kim; Korean J Pathol. 1988;22(4):383-392.

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Abstract PDF: To investigate the pathogenesis of the duodenal ulceration produced by mepirizole (1-(4-methoxy-6-methyl-2-pyrimidinyl)-3-methyl-5-methoxypyrazole) in rat, the effects of various concentraion and sorts of antiulcer drugs and truncal vagotomy on the mepirizole (200 mg/kg of body weight) induced duodenal ulcers were observed morphologically, and after mepirizole administration (200 mg/kg), amount and acidity of gastric jucie were measured sequently. The results were as follows: 1) In the control group of fasting for 24 hours after mepirizole administration only, duodenal ulcers were developed in all animals with 21.5+/-5.8 mm2 of ulcer index, perforation rate was 15%, and mortality rate was 0%. But lesions of the stomach were hemorrhagic and erosive with erosion index of 3.8+/-1.6 mm2. 2) The antiulcer drugs were significantly inhibited duodenal ulceration and gastric erosion produced by mepirizole although the inhibition effects were different. 3) After truncal vagotomy, duodenal ulcer and gastric erosion induced by mepirizole were also significantly inhibited. 4) On the gastric analysis, decrease of amount, increase of acidity, and decrease of concentration of gastric juice were observed after administration of mepirizole compared with nontreated normal group. Above findings suggest that the pathogenesis of the duodenal ulceration by mepirizole is the action of gastric acid on the duodenal mucosa with breakdown of defence mechanisms of the duodenum.

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