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

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

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

This study was carried out to investigate the ultrastructural findings of rats after administration of 0.5% lead acetate with drinking water. The Sprague-Dawley rats were divided into control and experimental groups. The control group was composed of 12 rats and was orally administered with 0.5% sodium acetate. The experimental group was composed of 36 rats and orally administered with 0.5% lead acetate. Two rats in the control group and four rats in the experimental group were sacrificed on day 2, and week 1, 2, 4, 6 and 8 after administration. The kidney was extirpated and examined by electron microscopy. The results obtained were as follows: The blood lead concentration in the experimental group began to increase from the second day after administration and it increased gradually until the 6th week and it decreased at the 8 week. The urinary excretion of delta-ALA also increased from the secondary and gradually increased up to the 8th week. On electron microscopic examination, the proximal tubular cells showed fat droplets, dilatation of the endoplasmic reticulum, mitochondrial swelling, increased numbers of secondary lysosomes and myelin figure-like residual bodies and intranuclear inclusion bodies. All these findings peaked at the eighth week after administration. Ultrastructural findings after Timm sulphide silver reaction revealed the lead granules in the proximal tubular lumen and between the microvilli of the proximal tubular cells without membrane-bounded. It can be concluded that most of the changes of micro-organelles are compatible with degenerative changes of lead exposure and passive diffusion of lead granules are involved in the proximal tubular cells.
Rats ; Animals

An experimental studies were carried out to observe the protective effects of malotilate, a new antihepatotoxic agent, on the chronic hepatic injury induced by CCl4 with or without ethanol. The rats used weighed about 200g were divided into 2 groups, 4 weeks & 8 weeks. Each group was given by orally with malotilate, 100 mg/kg, once a day, and was injected by subcutaneously with CCl4 1.5 mg/kg in a mixture with olive oil twice a week. Aqueous ethanol (20%) was administered in drinking water daily. The serochemical and histopathological studies were carried out in each experimental group. The results were as follows: 1. The chronic liver injuries induced by CCl4 with or without ethanol were significantly ameliorated by normalize serum values GOT, GPT. Alkaline phosphatase, Cholesterol, HDL-Cholesterol, and gamma glutamyl transpeptidase. 2. In Group of 4 weeks, malotilate manifested protective effects by significant inhibition of fatty changes, spotty necrosis and fibrosis in CCl4-intoxicated liver with or without additional ethanol. 3. In group of 8 weeks, malotilate significantly imoproved fatty changes, fibrogenic activity in the group administered with CCl4, followed by ethanol.
Rats ; Animals

No abstract available.
Animals ; Rats*

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.
Rats ; Animals

PURPOSE: To determine whether febrile seizure enhances neuroexcitability by altering synaptic transmission and whether febrile seizure-induced hyperexcitability leads to long-lasting neuronal death. METHODS: We investigated the expression of synaptic and postsynaptic proteins and the apoptosis of neuronal cells in rat pup hippocampus after hyperthermic seizure using immunoblotting and confocal microscopy. RESULTS: Hyperthermic seizure enhanced the long-term expressions of presynaptic proteins such as syntaxin, VAMP, SNAP-25 and nSec1, whereas that of NSF was decreased. The expressions of postsynaptic NMDA receptors 1, 2a and 2b were up-regulated. The expression of postsynaptic AMPA glutamate receptors 1 month after hyperthermic seizures altered by way of increasing the ratio of GluR1 to GluR2 and decreasing NSF-GluR2 interaction, which leads to the formation of Ca2+permeable AMPA receptors and enhanced toxicity. However, in spite of enhanced neuroexcitability, there was a transient increase of neuronal death in hipocampus one week after hyperthermic seizure, but returned to baseline one month later. CONCLUSION: These results demonstrate both presynaptic and postsynaptic forms of long-term enhancement of glutamate synaptic transmission after hyperthermic seizure and support the idea that early-life febrile seizure might have persistent effects on neuronal excitability in the hippocampus.
Rats ; Animals