• Korean Journal of Veterinary Research
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• v.22 no.2
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• pp.221-232
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• 1982

This paper dealt with the pathological and clinical findings on the experimentally induced rodenticide (fluoroacetate, zinc phosphide, thallium sulfate, coumarin) and NaCN poisoning of ruminants (Holstein cattle and/or Korean native goat) for the purpose of the diagnosis in the accidental rodenticide poisoning of cattle. The results observed are summarized as follows: Fluoroacetate poisoning (cattle and goat): in the clinical signs, there were depression, convulsion, dyspnea, groan, grinding of the teeth, vomiting, opisthotonus and post-mortem tympany. In the macroscopical findings, the blood was more or less poor coagulative and dark red, bloody fluid with foam in the trachea, hyperemia and hemorrhage of tracheal mucosa and lung, cloudy swelling and hyperemia of kidney, epicardial hemorrhage(cattle), and hyperemia of abomasum, intestine and brain were observed. In the microscopical findings, there were pulmonary edema and hemorrhage, necrosis of convoluted tubular epithelium and interstitial hemorrhage of kidney, focal coagulative necrosis of myocardium, hemorrhage of pancreas and spleen, dilatation of Virchow-Robin space and hyperemia of brain, and necrosis with desquamation of mucosal epithelia of abomasum and upper small intestine. In the histological lesions of the liver, lobular peripheral hyperemia, centrilobular necrosis and cytoplasmic inclusion bodies of the hetatic cells were observed. The cytoplasmic inclusion body of the hepatic cells was not seen in the affected goat, but hydropic degeneration of the hepatic cells was marked. Zinc phosphide poisoning (cattle and goat): clinically, the affected animals died in recumbent position after ataxia, dyspnea and convulsion. In the macroscopical findings, hyperemia and hemorrhage of lung, cloudy swelling and hyperemia of liver and kidney, hemorrhage of spleen (cattle), and catarrh of abomasum and small intestine were observed. In the microscopical findings, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hemorrhage of spleen, hyperemia of lung, hyperemia or hemorrhage of heart, cloudy. swelling and fatty changes of hepatic cells, dilatation of hepatic central vein, hyperemia of brain, and catarrh of abomasal and small intestinal mucosae were observed. Thallium sulfate poisoning (cattle): in the macroscopical findings dark red color of blood, hyperemia and hemorrhage of lung, bloody fluid with foam in the tracheal mucosa, petechiae of tracheal mucosa, cloudy swelling and hemorrhage of liver, necrotic lesions and hemorrhage of renal cortex and epicardial hemorrhage were observed. In the microscopical findings, severe hemorrhages of the lung, cloudy swelling and necrosis of hepatic cells, hyperemia and hemorrhage of liver, focal coagulative necrosis of mycordium, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hyperemia and hemorrhage of spleen and dilatation of Virchow-Robin apace in brain were observed. Coumarin poisoning (goat): the poisoned animals died in the state of groan and depression. In the macroscopical findings, poor coagulation of blood, hemorrhage of lung, cloudy swelling and severe hemorrhages of liver, cloudy swelling and hemorrhage of kidney, abomasal hemorrhage, catarrh of small intestine, and hyperemia and hemorrhage of the other organs were observed, In the microscopical findings, hyperemia and hemorrhage of lung and kidney, cloudy swelling of the convoluted tubular epithelium of kidney, severe hepatic hyperemia, cloudy swelling and hydropic degeneration of heptatic cell, and hyperemia and hemorrhage of brain and spleen were observed. NaCN poisoning (cattle and goat): clinically, there were convulsion, severe dyspnea, paresis of hind limb, depression and then rigor of four limbs. In the macroscopical findings, bright red color of blood, hyperemia and bright and red tinge of lung cloudy swelling of kidney and liver, and hyperemia of abomasum were observed. In the microscopical findings, cloudy swelling and hydropic degeneration of hepatic cell, hyperemia and edema of lung, necrosis and degeneration of the convoluted tubular epithelium and hemorrhage in kidney, dilatation of Virchow-Robin space of brain and hemorrhage of spleen were observed.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2002.11a
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• pp.141-141
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• 2002

A patient (Painter+Viszula mixed breed, 4 months old, male), with chief historic sign of acute vomiting, hemorrhagic diarrhea, anorexia and dyspnea during 4 days was admitted ta College of Veterinary Medicine, Kyungpook National University. Necropsy findings were revealed ulcer and hemorrhage contained hemorrhagic diarrhea in gastrointestinal tract, severe emphysema and hemorrhage in the lung and kidney and cardiac hypertropy. Histopathological changes showed emphysema, hyperemia and hemorrhage in the lung, severe hyperemia, hemorrhage, hepatic vacuolation and cellular necrosis in the liver, hyperemia, hemorrhage, necrosis of tubular epithelium in the kidney, hemorrhage in cardiac muscle and hyperemia, necrosis and sloughing of epithelium in the intestine. In this case, we diagnosed as a paraquat poisoning.

• Korean Journal of Veterinary Research
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• v.24 no.2
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• pp.127-136
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• 1984

The present study was carried out to observe the histological changes of the parenchymal organs of the rats, rabbits and dogs intramuscularly injected with Rompun. The results observed are snmmarized as follows; The hematologic changes of the rabbits and dogs administered with Rompun were a pronounced decrease in erythrocytes and leucocytes. The percentage of lympocytes was decreased, while that of neutrophils was increased. There were severe hyperemia of spleen, hyperemia and extention of the central vein of the liver, centrilobular degeneration of liver, hyperemia and hemorrhage of the kidney, necrosis and hydropic degeneration of renal tubule, hyperemia of pulmonary alveolar septa and pulmonary edema. and in the cases injected with Rompun and histamine or pentothal sodium at the same time, the microscopical findings described above were more conspicuous than the cases injected with Rompun alone.

• Journal of Veterinary Clinics
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• v.19 no.3
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• pp.379-382
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• 2002

A patient (Pointer+Viszula mixed breed, 4 months old, male), with chief historic sign of acute vomiting, hemorrhagic diarrhea, anorexia and dyspnea during 4 days was admitted to College of Veterinary Medicine, Kyungpook National University. Necropsy findings were revealed ulcer and hemorrhage contained hemorrhagic diarrhea in gastrointestinal tract, severe emphysema and hemorrhage in the lung and kidney and cardiac hypertropy. Histopathological changes showed emphysema, hyperemia and hemorrhage in the lung, severe hyperemia, hemorrhage, hepatic vacuolation and cellular necrosis in the liver, hyperemia, hemorrhage, necrosis of tubular epithelium in the kidney, hemorrhage in cardiac muscle and hyperemia, necrosis and sloughing of epithelium in the intestine. Histopathological diagnosis was made as paraquat poisoning.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.97-103
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• 1976

In order to clarify the histopathological changes resulting from nitrate poisoning, rabbits were experimentally poisoned by the oral administration of $KNO_3$ or $NaNO_2$ and examined clinically and histopathologically. In addition, the quantitative changes of glycogen level in hepatic cells were histochemically observed. The results obtained were summarized as follows: 1. Clinical symptoms observed from the acute cases which died within 2 hours after the administration were severe cyanosis of visible mucosa, frequent urination, and dyspnea. However, in chronic cases administrated daily with $KNO_3$ for 43, 50 and 74 days respectively, no marked symptoms were observed. 2. Macroscopic changes observed in acute cases were severe methemoglobinemia, cloudy swelling of hepatic cells, hemorrhage and hyperemia of gastric mucosa, and hyperemia of other organs. In chronic cases there were marked hyperemia, dark-red coloring and increasing of consistency in liver and kidney, and swelling of spleen. 3. Microscopic changes observed in acute cases were hemorrhage and hyperemia of various organs, cloudy swelling and centrilobular necrosis of hepatic cells and necrosis of convoluted tubular epithelium in kidney. In chronic cases there were round cell infiltration of the interlobular connective tissue and epithelial proliferation of interlobular bile ducts in the liver, and necrosis of the convoluted tubular epithelium and proliferation of interstitial connective tissue in kidney, thickening of alveolar septa of lungs, activated hemopoiesis of bone marrow, and myeloid metaplasia of sqlenic pulp. 4. Glycogen storage in liver cells was decreased in acute cases, on the contrary, increased in chronic cases.

• Proceedings of the KSMRM Conference
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• 2001.11a
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• pp.170-170
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• 2001

Purpose： To evaluate the relationship between reperfusion hyperemia in reversible cerebral ischem and the degree of programmed cell death. Method： We produced the animal models of reversible cerebral ischemia in 10 cats by mean of middle cerebral artery (MCA) occlusion with transorbital approach. MCA was occluded b microvascular clamp for an hour. MR imaging was performed at 0, 1, 2 days after ischemi and reperfusion. Perfusion (PWI) [Contrast enhanced GRE EPI, TR/TE= 1500/40, 40 Phases, 128 matrix, 12 cm FOV] and diffusion (DWI) (SE EPI, b=0, 500, 1000) weighted images were obtained using Philips Intera 1.57 system. rCBV and ADC maps were calculated wi IDL based postprocessing program. Tissue slices were obtained after the last MR imagin TUNEL, Calbin and Acid-Fuscin staining were done for corresponding slices as MR imagin We investigated the differences of degree of apoptosis in the area of reperfusion hyperemia.

• The Journal of Dong Guk Oriental Medicine
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• v.2 no.1
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• pp.19-54
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• 1993

To see both $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$(dissipate phlegm and promote vital energy circulation) and $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$(blood circulation and disperse blood stasis) influencing on thrombosis, contusion-hyperemia, and hyperlipidemia, at first we measured the density of FDP, the quantity of fibrinogen, prothrombin time, and the number of platelet of rat taken thrombosis by endotoxin. Secondly we measured the increase-rate of "paw swelling", the number of platelet, the quantity of fibrinogen, and prothrombin time of rat taken contusion-hyperemia. And then we measured the quantity of total cholesterol in serum and of H.D.L-cholesterol and of triglyceride and of phospholipid and of ${\beta}-lipoprotein$, its weight, and the variation of the quantity of electrolyte of rat taken hyperlipidemia by the oral-injection of choleserol. As a result, we can conclude as follows : 1. Out of the test of thrombosis, we can recognize not only the noticeable increae of the number of platelet and the quantity of fibrinogen, but also the noticeable decrease of prothrombin time and the density of FDP in case of $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$-injected rat and $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$-injected rat. 2. Out of the test of contusion-hyperemia, we can recognize not only the noticeable increase of the number of platelet and the quantity of fibrinogen, but also the noticeable decrease of prothrombin time and "increase-rate of paw swelling" in case of $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$-injected rat and $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$-injected rat. 3. Out of the test of hyperlipidemia, at first we can recognize that test rat's weight increased as close as that of normal rat. And we can recognize the noticeable decrease of the triglyceride and phospholipid and ${\beta}-lipoprotein$." Also, in case of the variation of electrolyte we can recognize the decrease of calcium and potassium in $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$-injected rat, and of sodium and magnesium in $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$-injected rat. Thus, as the above-mentioned, in covering thrombosis, contusion-hypermia, and hyperlipidemia, the effect of $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$ and $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$ can be recognized. Granting that $Hu{\grave{a}}y{\bar{u}}t{\bar{a}}ng$ reveals its effectiveness in thrombosis and contusion-hyperemia, and $Sh{\grave{u}}nq{\grave{i}}daot{\acute{a}}nt{\bar{a}}ng$ in hyperlipidemia, it can be inferred that contusion-hyperemia is like "model of blood stasis form" as thrombosis and hyperlipidemia "phlegm-retention diseases form", and both phlegm-retention and blood stasis have correlation each other.

• Proceedings of the KSLP Conference
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• 2015.03a
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• pp.24-24
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• 2015

• Korean Journal of Veterinary Research
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• v.27 no.2
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• pp.277-290
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• 1987

This paper dealt with etiological studies on the acute fatal disease of Angora rabbits occurring as a group in Korea. The disease was confirmed as an acute infectious disease caused by virus. The results obtained were summarized as follows: The disease produced a high morbidity in the rearing Angora rabbits and a high mortality in the infected rabbits, and was acute. The infected rabbits died soon without premonitory signs after inappetence. The body temperature of the affected rabbits rose to $40^{\circ}C$ and nearly all deaths occurred within 48 hours after inoculation. In many cases a bloody foam was visible from the nostrils after death. According to the progress of the disease the nervous signs, such as ataxia, paralysis of the legs, and torticollis could be recognized in the some cases. Rabbits that had recovered from the disease were severe emaciation, and bristly and sparse hairs. In macroscopical findings, there were hemorrhage and edema of the lung, hemorrhage or hyperemia of the tracheal and broncheal mucosae, appearance of blood-tinged effusion in the respiratory tract. The principal lesions were found in the liver. Usually the lobular necrosis of the liver cells was progressed, and focal necrosis and hemorrhagic spots of various sizes were often observed in the liver. Liver was as a whole pale. In chronic cases, however, there was a slight liver cirrhosis with the atrophy of the parenchymal cells. The other lesions encountered grossly consisted of swelling and petechiae of the kidney, hyperemia and hemorrhage of the spleen, catarrh of the small intestine, and hyperemia of the brain. The urinary bladder contained a lot of turbid urine or bloody urine and urinary cast, and was distended with the urine. In microscopical findings, the most striking lesions occurred in the liver and may be classified as viral hepatitis. The hepatic lesions were initially characterized by progression from periportal to peripheral necrosis of the lobules with the infiltration of mononuclear cells. Focal necrosis of various sizes, hemorrhage and hyperemia were often observed in the hepatic lobules. In chronic cases, there were intensive infiltration of lymphocytes, proliferation of fibroblasts, appearance of plasmal cells, and atrophy of parenchymal cells in the hepatic tissue. Perivascular lymphocytic infiltration and meningitis were seen in the brain and spinal cord. In the kidney, there were acute glomerulonephritis, hemorrhage, necrosis of the uriniferous tubules, and retention of eosinophilic substance within the renal tubules. Proliferation of fibroblasts and infiltration of mono-nuclear cells were found in the interstitial stroma of the kidney in chronic case. There were also hemorrhage and edema in the lung, hyperemia and hemorrhage in the trachea and bronchus, perivascular lymphocytic infiltration and focal myocardial necrosis in the heart, hyperemia and hemorrhage in the spleen, vacuolization and desquamation of mucous epithelia in the urinary bladder, catarrhal inflammation of the small intestine, hemorrhage in the adrenal cortex and hyperemia in the other organs. In the electron microscopical findings of the hepatic tissue, crystals of viral particles appeared in the cytoplasm of the hepatocytes and the sinusoidal endothelial cells, and the viral particles, were small in size and polygonal. The authors suppose the virus may belong to picornaviridae family of RNA viruses. Also immature virus-like particles, dilated rough endoplasmic reticulum and destruction of nuclear membrane were seen in the hepatocytes. From these results, it is concluded that the sudden death is an acute viral disease characterized by hepatitis and the affected rabbits may be died of viremia.

• Journal of Nutrition and Health
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• v.28 no.2
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• pp.115-126
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• 1995

The effects of energy-yielding substrates on coronary circulation, myocardial oxygen metabolism, and intramyocytic adenylates of perfused Wistar control rat(WC) and spontaneously hypertensive rat(SHR) hearts were examined under basal and $\beta$-adrenergic stimulation conditions. The perfusion medium (1.0mM Ca2+) contained 5mM glucose (+5U/l insulin) in combination with 5mM pyruvate, 5mM lacate, 5mM acetate, or 5mM octanoate as energy substrates. Hearts were perfused with each substrate buffer for 20min under basal conditions. Coronary functinal hyperemia was induced by infusing for 20min isoproterenol (ISO, 1uM), a $\beta$-receptor agonist. Cardiac adenylates, glycolytic intermediates, and coronary venous lactate were measured by using an enzymatic analysis technique. Under basal conditions, acetate and octanoate significantly increased coronary flow(CF) of WC in parallel with myocardial oxygen consumption. However, CF of SHR was partly attenuated by coronary vasoconstriction despite metabolic acidosis. In addition, pyruvate and lactate depressd ISO-induced coronary functional hyperemia in SHR. It should be noted that octanoate exhibited coronary dysfunction under ISO conditions. On the other hand, fat substrates depleted myocardial high energy phosphate pool and accumulated breakdown intermediates. In SHR with coronary vasoconstriction under basal conditions, and with depressed coronary functional hyperemia, high energy phosphates were greatly depleted. These results suggest that energy substrates in the myocardium and coronary smooth muscle alter remarkably coronary circulation, and that coronary circulatory function is associated with a reserve of high energy phosphates and a balance between breakdown and nono synthesis of energy phosphates. These findings could be explained by alterations in the cytosolic redox state manipulated by LDH and hence in the cytosolic phosphorylation potential, which might be involved in hypertension of SHR.