No abstract available.
Animals ; Rats*

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.
Rats ; Animals

This study was carried out to investigate the mechanisms of interstitial pulmonary fibrosis of rats after the intratracheal administration of bleomycin. Both lungs after bleomycin injection were examined by light and electron microscopy. The results are as follows: Light microscopically, 1 or 2 weeks after bleomycin injection acute and chronic inflammatory infiltrates and edema in the interstitium and alveolar spaces were observed. Proliferation of alveolar type II pneumocytes was also found at 4 to 6 weeks after bleomycin injection, chronic inflammatory infiltrates with interstitial fibrous thickening were noted. Electron microscopically, the number of type II pneumocytes and irregular lamellar bodies were increased and blunted microvilli were noted at 2 weeks. 4 to 8 weeks, proliferation of fibroblasts with deposition of abundant collagen fibrils in the thickened interstitium revealing irregular or collapsed alveolar spaces were observed. Based on these findings, it can be concluded that bleomycin-induced interstitial pulmonary fibrosis is considered to pass from an early acute inflammation of the interstitium and alveolar spaces to an interstitial fibroblast proliferation and collagen deposition to the length of the period after injection.
Rats ; Animals

The authors studied the formation of giant mitochondria in liver cell. The Sprague Dawley rats were sacrificed following intervals; 5, 10, 20, 30, and 60 minutes after intraperitoneal injection of hydrazine in the amount of 200 microliter/kg. And the extracted liver tissues were examined with light and electron microscopes. The results obtained were summarized as follow; Light microscopically, there is little difference between control and experimental groups. Electron microscopically, elongated, bizzare shaped mitochondria are appears 5 minutes after hydrazine injection. Those show attenuated portion, Y, U, or C shaped feature suggesting fusion or budding mitochondria. The number of giant mitochondria is decreased after 10 minutes group and rarely present in 60 minutes group. The results suggest in this experiment that the formation of giant mitochondria is kind of reversible change and it is different from the mitochondrial swelling of cellular injury. Intermitochondrial fusion and mitochondrial budding may be related with the formation of giant mitochondria.
Rats ; Animals

The purpose of this study is to investigate the morphologic changes of the sinusoidal endothelial cells and the associated structures of the cirrhotic rat liver induced by repeat intraperitoneal injections of N-diethylnitrosamine (DEN) (100 mg/kg/week). One day to 6 weeks later, rat livers were observed under the light, transmission and scanning electron microscopy, and immunostained with laminin antibody. Two weeks after DEN treatment, the fibrillar material in Disse's space was noted, and then a basement membrane-like structure was found at 4 weeks after treatment. Laminin was detected in perisinusoidal areas after 4 weeks. Laminin was strongly positive on the fibrous septum and in the sinusoidal wall of cirrhotic nodules after 6 weeks of treatment. The diameters and numbers of sinusoidal endothelial fenestrations did not change significantly until 2 weeks. They decreased within 4 weeks, and then the sinusoidal endothelium was poorly fenestrated at 6 weeks after DEN treatment. These results suggest that as fibrosis develops in cirrhosis, the deposit of extracellular matrix such as laminin within Disse's space is a major contributing factor in the structural alteration of sinusoidal endothelial cells, and the capillarization of the sinusoidal endothelial cells may be a contributor to impairment of the hepatic function in cirrhosis.
Rats ; Animals

No abstract available.
Animals ; Rats*

No abstract available.
Animals ; Rats

To investigate the mechanism of monocrotaline-induced pulmonary arterial hypertension, authors performed immunohistochemical study using antibody to von Willebrand factor(vWF), cell kinetic study using 5-bromodeoxyuridine and ultrastructural study after single subcutaneous injection of monocrotaline(MCT) to Wistar rats. The results of this study demonstrated that the expression of vWF by pulmonary endothelial cells was markedly increased from day 3 until 2 months after MCT injection. The labeling index of pulmonary microvessel endothelium began to increase after six days and was maximal on the third weeks, and thereafter it remained slightly increased above basal level. Electron microscopic study revealed attachment of inflammatory cells an platelets to endothelium from 6 hours and degranulation of attached platelets 24 hours after MCT injection. Evidences of endothelial injury began to appear from 12 hours after MCT injection. Evidences of endothelial injury began to appear from 12 hours and was maximal after 48 hours. From the third day, ultrastructural change of cell regeneration and hypertrophy began to appear and was continuosly observed until 2 months. In addition, we evaluated the changes in the number of pulmonary neuroendocrine cells using antibody to gastrin releasing peptide but it demonstrated no change until 2 months suggesting no role of neuroendocrine cells in the development of pulmonary hypertension of Wistar rats at early stage. In conclusion, the results indicate that pulmonary hypertension by MCT injection is due to increased vascular resistance caused by vasoconstriction and hyperplasia of endothelium with musculariz ation of the pulmonary arterioles induced by endothelial dysfunction and some biologic substances released form endothelium and platelets.
Rats ; Animals

The toxicity and adrenostatic effect of o,p'-DDD, a derivative of the insecticidal DDT, on the adrenal cortex were well known. It known that the toxicity was based on the blocking of steroid biopsynthesis when cholesterol was converted to pregnenolone. Lysodren(R) was also known to be capable of producing a regression of adrenocortical carcinoma and its metastases, and this drug became one of useful choice for the treatment of unoperable adrenocortical carcinomas. Recently, fine structural effect of o,p'-DDD on the adrenocortical carcinoma show that the mitochondria is the primary target organelle. o,p'-DDD was dissolved in corn oil and it was orally administered for 28 days to investigate the ultrastructural effects of zona fasciculata of rat adrenal cortex. The results obtained were as follow: 1) The body weight was decreased after feeding o,p'-DDD. 2) Light microscopic examination showed no remarkable change except increased fine lipid droplets of zona fasciculata in group I (o,p'-DDD 75 mg/kg feeding). Moderately increased intracytoplasmic lipid droplets and pyknotic nuclei bearing membrane indentations were seen in group II (o,p'-DDD 150 mg/kg feeding). Large sized lipid droplet aggregates, pyknotic nuclei with severe nuclear membrane indentations and karyorrhexis in focal area were evident in group III. 3) Immunohistochemical staining for ACTH in pituitary gland showed increasing number of ACTH secretory cell and increasing intensity of staining property according to the dosage of o,p'-DDD. 4) Ultrastructural examination showed increased intracytoplasmic lipid droplets and mild increased peroxisome. There was no remarkable ultrastructural changes in mitochondria in group I. Moderately increased lipid droplets and clusters formation, compressed mitochondria, partial disappearance of mitochondrial cristae, increased peroxisome and nuclear membrane indentations were seen in group II. In group III, nuclear membrane showed prominent indentation. Numberous cytoplasmic vacuolation, double membrane ring in mitochondria, disappearance of mitochondrial cristae, myelin figure formation in mitochondrial matrix, and fatty changes in mitochondrial matrix were seen. These findings showed that the primary target organelle of attack by o,p'-DDD on zona fasciculata of adrenal gland in rat is mitochondria and it was developed from double ring formation in mitochondrial matrix.
Rats ; Animals

In an attempt ultrastructural study of alcohol-induced gastric mucosal change, we selected sixty Sprague-Dawley rats. The rats were administrated with 4 ml of 10% and 40% ethanol enterically and examined by light and electron microscopy. Light microscopically, the thickness of the mucus layer of both 10% and 40% ethanol groups was decreased. The antral mucosa revealed focal inflammatory infiltrates, disturbed glandular arrangements, and significant decrease of mucosal thichness and proper glands. On scanning electron microscopy, flattened or swollen mucosal epithelium and irregularly distributed gastric pits were seen in both experimental groups, and these changes were more severe in the groups of higher concentration and longer duration. On transmission electron microscopy, mitochondrial abnormalities with myelin-like materials and dilatation of endoplasmic reticulum and cytoplasmic blebs were observed. Also the mucus cells show significantly decreased mucus globules, increased fat vacuoles, and large autophagic vacuoles. These alterations were similar to those produced by ethanol in the liver and small intestine. This study indicates that, prolonged administration of ethanol induced chronic gastritis, especially chronic atrophic gastritis.
Rats ; Animals