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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General pharmacological effects of [Ethyl p-(6-guanidinohexanoyloxy)benzoate] methanesulfonate (FOY), a new antiproteolytic agent, were studied and the following results were obtained. Acute administration of large doses of FOY in conscious dogs and rabbits caused a decrease in spontaneous motility, ataxia, cyanosis, collapse, mydriasis, and respiratory paralysis. The agent had no effect on the central nervous system and exhibited hypotensive effects in dogs in doses of more than 1 mg/kg. Hypotensive responses were not inhibited by treatment with atropine or hexamethonium. FOY had no effects on ECG in the rabbit at doses of less than 30 mg/kg and at doses from 10(-6) to 10(-4)g/ml, distinctly reduced the amplitude of the spontaneous and rhythmic contractions of the isolated rabbit ileum, guinea-pig ileum and rat uterus preparation. The contractile response to nerve stimulation, noradrenaline and barium was suppressed in isolated guinea-pig vas deferens. FOY had no effects on the twitch response of gastrocnemius muscle to sciatic nerve stimulation in rats. The drug caused local irritant effects in rabbits and rats.
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PMID:[Pharmacological action of [ethyl p(6-guanidinohexanoyloxy)benzoate] methanesulfonate (FOY)]. 23 87

Twenty-seven sheep were assigned to three groups in order to study acute urea toxicity. Groups I, II and III were dosed with 0.5, 0.6 annd 0.75 g/kg of urea, respectively. The mean survival times were 165, 109 and 60 minutes, respectively. The following clinical signs such as pronounced muscle fasciculation, trembling, grinding teeth, ataxia, lateral recumbency, bloating, regurgitation, hyperesthesia, mydriasis and convulsions were observed. Anuria and lack of salivation were also present. The primary cause of death in this study was due to respiratory arrest and not cardiovascular collapse. Plasma examinations showed a marked increase in glucose, ammonia and urea levels but no change in ketone body concentration.
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PMID:Acute urea toxicity in sheep. 64 59

The physical and mental reactions were registered before and after smoking 2 g hashish in 30 volunteers who had never smoked hashish before. The EEG shows no pathological changes. Hashish significantly raises the heart rate. The blood pressure shows a tendency to fall. The cardiovascular disturbances may be so marked that collapse occurs. The reaction of fear after acute hashish intoxication may lead to unpleasant defense reactions. Hashish implies a danger to road traffic because of the physical ataxia and alterations in appreciation of time and space.
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PMID:[Clinical and electroencephalographic observations during the acute action of hashish (author's transl)]. 80 10

The clinical features and pathological findings of 6 steers drenched with dried plant material of Cestrum laevigatum are described. Doses ranging from 0.5 to 10 g/kg/day were given intraruminally for 1 to 38 days. Animals that received 5 to 10 g/kg/day showed nervous signs including ataxia, muscle tremors, hypersensitivity and intermittent chewing. Clinical signs in the steers which received 0,5 to 4 g/kg/day were mild. High doses induced moderate to severe hepatosis characterized by centrilobular to midzonal coagulative necrosis, haemorrhage and congestion. At lower rates only mild hepatic lesions, characterized by disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas were evident. Ultrastructural changes were primarily limited to the hepatocytes and comprised degeneration, necrosis and fatty change. Degeneration and necrosis of endothelial cells and disruption of sinusoidal walls were occasionally observed.
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PMID:The pathology of Cestrum laevigatum (Schlechtd.) poisoning in cattle. 192 85

Patent ductus venosus was diagnosed in a 10-week-old Holstein heifer with acute onset of collapse and marked tenesmus. Additional clinical signs observed during the course of hospitalization included depression, anorexia, hind limb ataxia, bruxism, and poor growth. Clinicopathologic test results included high blood ammonia concentration, prolonged sulfobromophthalein half-life, and high serum bile acid concentration. Liver biopsy revealed mild periportal fibrosis, but no appreciable hepatocyte atrophy. Mesenteric portography and percutaneous ultrasonography confirmed the patent ductus venosus. An atrial septal defect prosthesis was placed in the ductus venosus, using a catheterization technique. After surgery, however, clinicopathologic test results were unchanged. Ultrasonography revealed that the prosthesis had pulled away from one side of the vessel. When the calf was 10.5 months old, surgical correction was achieved by a transhepatic ligation technique. Ultrasonography confirmed closure of the ductus venosus during and after surgery. Blood ammonia and serum bile acid concentrations and sulfobromophthalein half-life were normal 3 weeks after surgery. The calf had no further episodes of hepatoencephalopathy and was successfully bred at 18 months of age.
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PMID:Diagnosis and surgical correction of patent ductus venosus in a calf. 306 3

Reaction to rapid intravenous administration (RIA) of rifampicin in a dose of 10 mg/kg was studied on 173 healthy dogs. Immediately after the first RIA of rifampicin there were observed vomiting and ataxia of various levels in 5.2 per cent of the animals. After the drug administration their arterial pressure (AP) lowered to 50-60 mm Hg. By the 9th-11th minute it restored to the initial level. A collapse-like condition was recorded immediately after rifampicin RIA in 2.3 per cent of the dogs with marked decreasing of their AP up to 15-20 mm Hg. Its restoration to the initial level was slow and required 35-40 min. It was noted that after the third consecutive RIA of rifampicin the observed reaction disappeared. Probably this was due to adaptation of the host to rifampicin intravenous injections. Mezaton is an efficient agent rapidly arresting the reaction within 1-3 min.
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PMID:[Complications and their elimination during the rapid intravenous administration of rifampicin in an experiment]. 367 42

Approximately 250 sheep were poisoned and died from ingesting death camas (Zygadenus paniculatus) within a 2-day period on a foothill range in southeastern Idaho. Sixty to 70% of the poisoned sheep were 80-90 lb lambs and the rest were mature ewes. Poisonings were confirmed by field investigation, microhistological analysis of plant fragments from rumen contents of dead sheep, clinical signs, gross and microscopic analysis of tissues, and by experimentally feeding death camas collected on the poisoning site to 3 ewes at the Poisonous Plant Research Laboratory at Logan, UT. Clinical signs and gross and microscopic analysis of tissues were similar in ewes from the field investigation to those in ewes experimentally fed death camas. Ataxia, muscular weakness, trembling, incoordination, discharge of frothy saliva from the mouth and nose, vomition, dyspnea, collapse and death were the most common clinical signs. Gross changes included severe pulmonary congestion and subcutaneous hemorrhage. Microscopic lesions were those of severe pulmonary congestion.
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PMID:Death camas poisoning in sheep: a case report. 382 76

Six foals of three different breeds, born to healthy mares, appeared normal at birth, and died at two to five days of age with icterus, ataxia, head pressing, and terminal hepatic coma. Their livers were less than one-half normal weight. Most of the liver was dark red-brown and slightly rubbery. Histologically, these areas were characterized by severe bile ductule proliferation, mild portal tract fibrosis, and massive hepatocellular necrosis and lobular collapse. A small proportion of the liver, usually on the peripheral part of the lobes, was grossly light brown and slightly raised. Histologically, these areas had mild to severe bile stasis in canaliculi. In the thin marginal zone between the severely affected and mildly affected liver, there was mild bile ductule proliferation and periportal fatty change and necrosis. Alzheimer's type II cells, characteristic of hepatoencephalopathy, were numerous in the brains of all foals. Within two hours after birth, all the foals had been given an oral proprietary nutritional paste, the ingredients of which included a viable Aspergillus sp and an iron compound. Similar lesions were produced in an experimental foal.
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PMID:Toxic hepatopathy in neonatal foals. 671 Aug 9

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

The fungus, Cladosporium trichoides, was isolated and cultured from a lesion in the cerebellum and from smaller lesions in the liver, kidney and spleen of a dog which had a history of behavioural changes, ataxia and collapse. Histopathological examination showed the cerebellar lesion to be a purulant granuloma which contained brown, septate hypae and structures resembling conidia. The source of infection was not traced and no predisposing factors were apparent. As far as is known, this is the first record of the condition in animals in southern Africa and the first report anywhere of this condition in the dog.
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PMID:Cerebral mycosis in a dog caused by Cladosporium trichoides Emmons 1952. 745 35


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