2.Serotonin Changes in Specific Brain Regions of Fibromyalgia Animal Model after Deep-sea Water Drinking.
Seong Ho KIM ; Nan Hee CHOI ; In Sick PARK ; Kyung Soo NAM
The Journal of the Korean Rheumatism Association 2008;15(2):110-117
OBJECTIVE: The acidic saline animal model of pain has been suggested to mimic fibromyalgia (FM). In this model, repeated intramuscular (IM) injections of acidic saline produce a widespread hyperalgesia that persists without evidence of significant peripheral tissue damage or inflammation, and is believed to be centrally maintained. We examined the changes of pain-related neurotransmitters in specific brain regions of this model after deep-sea water (DSW) drinking. METHODS: Rats were injected with 100microliter of acidic saline (pH 4.0) at days 0 and 5 into the left gastrocnemius muscle. Control rats received identical injections of physiological saline (pH 7.2) on the same schedule. Two acidic saline rats were given DSW from 1 week following the last IM injection to sacrifice. All rats were sacrificed on day 20. All regions of interest were examined for the changes of pain-related neurotransmitters with immunohistochemistry. RESULTS: Preliminary results showed that compared to controls, acid injected rats demonstrated strong expression of serotonin in red and raphe nucleus. Acid injected rats showed significant reductions of the serotonin expression in red and raphe nucleus after DSW drinking. CONCLUSION: IM acid injections increased the expression of serotonin in red and raphe nucleus of rats. The overwhelming reduction of serotonin expression in the nuclei after DSW drinking suggests DSW might be helpful for pain and anxiety. These preliminary data support the validity of acidic saline treatment as a model of FM, and provide a foundation for future analyses of specific brain regions that contribute to this syndrome.
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3.The Charateristics of Glycogen Metabolism of Diaphragm in Rats.
Bok Hyun NAM ; Eun Jung KIM ; Suck Kang LEE
Yeungnam University Journal of Medicine 1997;14(1):46-52
Diaphragm is though to play the most role in breathing and has a substantially greater proportion of slow oxidative and fast glycolytic fibers, and low proportion of fast oxidative fibers. The respiratory muscle, diaphragm, has the functional characteristics of slow speed of contraction, high resistance to fatigue and the ability to respond to intermittent ventilatory loads, for example of exercise. In the present study, the characteristics of the metabolism (depletion and repletion) of glycogen and the structural changes of diaphragm during depletion and repletion of glycogen were observed in rats. For comparison, the red gastrocnemius muscle which has a greater proportion of fast oxidative glycolytic (FOG) and slow oxidative (SO) fibers, and low proportion of fast glycolytic (FG) fiber, was also studied. The glycogen concentration of diaphragm in overnight fasted rats was 2.30+/-0.14mg/gm wet weight. The values of glycogen concentration at 60, 90 and 120minutes of treadmill exercise loaded rats was significantly decreased compared to that of the overnight fasted rats. There was no significant difference among the glycogen concentration of diaphragm at 60, 90 and 120minutes of exercises. The glycogen concentration of diaphragm was decreased to 1.12+/-0.17 from 2.30+/-0.14mg/gm wet weight by treadmill exercise. The glycogen depletion rats of diaphragm during exercise was faster than that of red gastrocnemius in both of the first 60minutes and 120minutes duration of exercise. The glycogen repletion of diaphragm after intragastric glucose administration by stomach tube was studied in control and exercise groups. The glycogen concentration was significantly increased after glucose administration in both of the control and exercise groups. All of the concentration of exercise group at 60, 120 and 180minutes after glucose administration was significantly higher than those of control group. In conclusion, one of the characterics of diaphragm in glycogen metabolism is fast glycogen depletion during exercise, and slowness of glycogen repletion after glucose ingestion in rats.
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5.Phospholipidosis of Liver Induced by Amiodarone.
Dong Hoon KIM ; Gium Mi JANG ; In Soo SUH ; Tae Joong SOHN
Korean Journal of Pathology 1991;25(1):1-10
Ultrastructural study of the effects of amiodarone on the liver tissue was performed. Rats were fed with amiodarone containing diet and were sacrificerd at 1st, 3rd, 4th, 5th and 8th weeks of experiment. Charateristic lisosomal inclusion bodies were appeared form first week, which were more prominent and increased in size at the 5th and 8th week of experiment. These inclusion bodies were found in hepatocytes, Kupffer cells, bile duct epithelial cells and fibroblasts but most prominent in hepatocytes. The lysosomal inclusion bodies could be divided into four types; those characterized by (1) dense bodies with packed crystaloid contents, (2) multilamellated bodies, (3) irregular shaped bodies with varying electron density and 4. dense bodies containing stacks of fine membranous structures. All types were found in all experimental groups. But the type 1 and 2 were predominent at early stage, while type 3 and 4 were more prominent at later stage According to these findings, the formation of the lysosmal inclusion body was a characteristic change in derangement of phospholipid metabolism. And amiodarone could induce disturbance of phospholipid metabolism in all kinds of cells in liver tissue.
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6.The Effect of Common Bile Duct Ligation on Liver Morphology and Coper Metabolism in Rat.
Kyoung Sook KIM ; Chanil PARK ; Jang Whan CHO ; In Joon CHOI ; Yoo Bock LEE
Korean Journal of Pathology 1990;24(4):402-411
To clarity the effect of biliary obliteration on copper metabolism of rat liver and on the hepatic morphology, 0.5% cuppuric sulfate was administered intraperitoneally for 42 days following ligation of the common bile duct (CBD) of Sprague-Dawley rats. The blood copper concentration, the hepatic copper content and the accumulation patterns of copper and copper binding protein in the liver were examined and compared with those of the simple CBD ligation group and the simple copper over loaded group. CBD ligation induced marked proliferation of bile ductular structures which, after expanding the portal tracts, invaded and divided the hepatic lobules. There was, however, no excess fibosis beyond what needed to support the new ductules. The blood copper concentration and the hepatic copper content were increased by copper overload with or without CBD ligation, particularly incases with CBD ligation. Liver cell necrosis did not occur by the overloaded copper alone in rats. The hepatic copper and copper binding protein were accumulated at periportal liver cells in the group of coppe overload after CBD ligatio, whereas they began to appear at perivenular hepatocytes in the simple copper overloaded group. In conclusion, it is suggested that CBD ligation does not induce excess fibrosis or liver cirrhosis in rat as far as during our experimental period, but affect significantly on copper metabolism by intrahepatic redistribution of the copper and the copper binding proteins.
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7.Ultrastructural Studies of Aortic Endothelial Injury and Regeneration.
Gium Mi JANG ; Dong Hoon KIM ; Jyung Sik KWAK ; Tae Joong SOHN
Korean Journal of Pathology 1990;24(4):337-348
Author performed this experiment to define the most important factor preventing the intimal thickening. An endothelium of abdominal aorta in the rat was denuded by two different wires having same caliver. The degree of injury was limited to the endothelial cells in one, and extended to the internal elastic lamina in another. The results showed that at 72 hours, in the case of superficial injury, the entire injury site was covered by new regenerating cells, but in the case of disruption of the internal elastic lamina, the migrating smooth muscle cell completely reached into the intima and resulted in intemal thickening. Similar findings persisted to 1 week later. Above results suggest the most important factor preventing the intimal thickening in endothelial injury is the depth of the injury which limited within the endothelial cells without extending into the internal elastic lamina and medial smooth muscle cells.
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8.Ultrastructural Changes of Lead Acetate Induced Liver Injury in Rats.
Korean Journal of Pathology 1996;30(3):184-198
To evaluate the ultrastructural changes and the mechanism causing liver injury by lead, light and electron microscopic(LM and EM) examination using Timm sulphide silver method(TSM) was done. Sprague-Dawley rats were divided into a control and 3 experimental groups. The experimental groups were orally administered 0.5% lead acetate(LA). Group 1 received a one time dose of 10 ml of LA by gastric intubation. Groups 2 and 3 continuously received LA instead of drinking water. The control group was composed of 3 rats in each group which did not receive any treatment. Rats of group 1, 2 and 3 and control were sacrificed at 1/2, 1, 1 1/2 hours, 2 days, and at 1, 2, 4, 6 and 8 weeks later, except group 3. Before sacrifice, they were perfused with 0.1% sodium sulphide and 2.5% glutaraldehyde through the abdominal aorta for TSM. The liver was taken for LM and EM examinations. Blood lead concentration began to increase from the 2nd day up to 3.29 microgram/ml at 2nd week, and the urinary delta-ALA level showed a steady increase from the 2nd day. LM and EM examination of liver revealed that absorbed lead granules in group 1 were transported into sinusoidal spaces, Kupffer cells, and the hepatocytes within 1 hour and then disappeared 1/2 hour thereafter. In group 2 deposited lead was found in the hepatocytic cytosol bound to mitochondria. That in turn inhibited mitochondrial respiration with resultant mitochondrial swelling at the 1st week and thereafter at 6th week myelin figure formation and condensation of mitochondria, and peroxisomes were increased at 8th week. Based on these results it can be concluded that a transient intake of subletal dose of LA is biotransformed completely by periportal hepatocytes within 1 1/2 hours, but excessively accumulated lead can induce liver cell injury due to lipid peroxidation of membrane by direct toxic effect of lead and by products of lipid peroxidation. We postulate that lead acetate triggers presumably primarily mitochondrial membrane injury and then other organellar changes may play a role in disturbance of a network of interacting of key events capable of causing cell death.
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9.Ultrastructural Changes of the Bile Canaliculi after Common Bile Duct Ligation.
Kook Seon YOO ; Suk Hee LEE ; Hee Kyung PARK ; Chang Ho CHO ; Jong Min CHAE
Korean Journal of Pathology 1996;30(3):175-183
The purpose of this study was to investigate the morphologic changes of the bile canaliculi and its associated structures of the liver induced by common bile duct ligation(CBDL) in the rat. The canalicular surface and lateral surface of the dry-fractured hepatocytes was studied with scanning electron microscopy at 1~6 weeks post ligation. The first week after CBDL, the bile canaliculi were dilated. The microvilli were increased in number and the lumens contained granular materials After 2 weeks or more, the bile canaliculi were dilated to a variable degree, and with irregularity, measuring from 1.5 to 5 micrometer in diameter, and in the advanced stage, the canaliculi showed blunting and the disappearance of microvilli. Some canaliculi had sprouting side branches. At 4~6 weeks post-ligation, the lateral surface of the hepatocytes also showed some irregularity and a tortuous appearance, and numerous small sized microvillous projections were formed. The tubular structures of the proliferated SER distributed adjacent to the lateral surface of the hepatocytes, and the direct connection of a tubular structure and the cytoplasmic membrane was observed. These results suggest that the deformity and loss of microvilli of bile canaliculi reflect the disturbance of bile secretion from the hepatocytes. And prolonged obstruction of bile flow may result in bile excretion via the lateral surface of hepatocytes.
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10.A Scanning Electron Microscopic Study on Microvascular Changes in the Monocrotaline-induced Rat Lung by Corrosion Casting Method.
Korean Journal of Pathology 1995;29(5):644-659
To investigate the microvascular changes in primary pulmonary hypertension, the lungs of 24 Sprague-Dawley rats were treated by an intraperitoneal injection of 2% monocrotaline(MCT) solution and then examined with scanning electron microscopy(SEM) after microvascular corrosion casting. Histologic examination revealed significant medial thickening in the small to medium-sized pulmonary arteries. Scanning electron microscopic findings of the normal lungs showed two kinds of microvascular structures. One showed a well-fortned three-dimensional basket structure of uniform flat-tubular alveolar capillaries, which were connected to each other in a T or Y shape or at right angles. The other revealed a two-dimensional reticular sheet of round tubular branches mainly in the bronchial artery-supplying regions. The MCT-treated groups(remodelling) showed apparent changes in both kinds of microvasculatures in comparison to the normal group but the more prominent change was found in Lbe bronchial artery microvasculature showing the dense thick encasement around large pulmonary arteries. Alveolar microvasculature of the pulmonary artery revealed individually enlarged angular appearance, with generally deformed alveolar architecture. Quantitatively, the significant enlargement of diameter and intercapillary distance appeared in both microvasculatures of MCT-induced rat lungs, but the density was increased only in the bronchial artery microvasculature. In conclusion, our three-dimensional microvascular study of the MCT-treated rat lungs demonstrates a new morphologic finding of vascular remodeling in primary puhnonary hypertension, which is thought to play an important vascular role in the pathogenesis in addition to interstitial fibrosis.
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