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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day X 6 days). Diminished treadmill test performance after 4 days of treatment marked the initial detection of impaired motor function. At this time fading (loss of tension during tetanus) of gastrocnemius contractions elicited in response to 100-Hz sciatic nerve stimulation occurred in DTB-treated rats but not in controls. After 5 and 6 days of treatment, treadmill failure became complete, tetanic fade worsened dramatically, and peak contractile tension measured during trains of nerve stimulation (10-250 Hz) decreased progressively. Appearing by Day 6 were marked body weight loss, dehydration, hypothermia, and a depression in serum concentrations of thyroid hormones. Total oxygen content of the blood was not reduced at any time during treatment, and serum concentrations of glucose, sodium, potassium, calcium, chloride, and phosphorus in DTB-treated rats on Day 6 were similar to those of control animals. Therefore, hypoxia, hypoglycemia, or a serum electrolyte imbalance do not initiate or modulate the neuromuscular toxicity. Light microscopic evaluation of liver, kidney, lung, thyroid, and other organs in intoxicated rats was unremarkable and in skeletal muscles and selected sites of brain, spinal cord, and sciatic nerve no morphologically significant lesions were observed. Even when DTB-intoxicated rats were maintained in a state of flaccid muscle weakness for 5 continuous days, peripheral nerve lesions proximal to the intramuscular nerves were not detected. Thus, depressed neuromuscular transmission appears to be the primary cause of the flaccid muscle weakness and no evidence was obtained that nonneural effects of DTB initiate or modulate this effect.
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PMID:Temporal analysis of dithiobiuret neurotoxicity in rats and assessment of potential nonneural causes. 311 11

The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
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PMID:Acute renal failure following nontraumatic rhabdomyolysis. 323 37

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

Rats were treated with amiodarone (20 mg/kg/day) up to 6 weeks and the neurotoxicity was assessed by determining changes in motor coordination, pain-threshold and rectal temperature every week during treatment. Body weight gain was decreased during amiodarone treatment and it was significant at and after 5 weeks. Food intake and water consumption were significantly reduced during treatment. After the first week of treatment with amiodarone, rats showed decreased ability to balance on horizontal rods. In the hot plate test (paw-lick), the amiodarone treated rats showed increased pain-thresholds throughout the treatment. Hypothermia was significant only at 6 weeks. These results show that amiodarone causes toxicity in rats and this model might be useful for further studies. Decreased motor-coordination, and increased pain-responding times may indicate development of peripheral neuropathy in addition to muscle weakness.
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PMID:Neurotoxicity in rats following subchronic amiodarone treatment. 371

Electrophysiological aspects of thiamine depletion in the rat induced by dietary deficiency are described. Behavioral changes as well as qualitative and quantitative alterations in the sensitivity of cerebellar Purkinje cells to iontophoretically-applied 5-hydroxytryptamine (5-HT) were observed. Thiamine-deficient rats were characterized essentially by ataxia, piloerection, paresis, apparent weakness, and hypothermia after 4-6 weeks on a thiamine-free diet. Basal Purkinje cell firing frequency was unaffected by thiamine deficiency. The response of Purkinje cells to iontophoretically-applied 5-HT was solely inhibitory in deficient rats. In control rats, however, responses to 5-HT were excitatory, biphasic, or inhibitory. Neurons in the thiamine-deficient animals were more sensitive to the inhibitory effects of 5-HT, as demonstrated by a significant parallel shift to the left of the dose-response curve. Durations of 5-HT effects were similar in both groups. Dose-response relationships for GABA-induced inhibition of Purkinje cell firing from thiamine deficient and control rats did not differ from one another. These data demonstrate a relatively selective effect of thiamine depletion on cerebellar serotonergic neurotransmission assessed electrophysiologically. We believe there is up-regulation of 5-HT receptors on Purkinje cells caused by thiamine deficiency-induced impairment of indoleamine input to the cerebellum from raphe and related nuclei.
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PMID:Enhanced sensitivity of cerebellar Purkinje cells to iontophoretically-applied serotonin in thiamine deficiency. 398 3

Two cases of Yersinia enterocolitica septicemia occurred in a breeding group of 22 adult patas monkeys (Erythrocebus patas). Affected animals had acute clinical signs of depression, weakness, dehydration, hypothermia, hepatomegaly and pronounced leukopenia. Both animals died a few hours after treatment was initiated. Gross necropsy findings included jaundice, fluid in body cavities, hepatomegaly, splenomegaly, multiple white foci within the liver and spleen, generalized lymph node enlargement and numerous mucosal ulcerations in the colon. Primary histopathological lesions were multifocal hepatic necrosis, splenic necrosis, chronic ulcerative enteritis and diaphragmatic myositis with necrosis and edema. Yersinia enterocolitica was cultured from the liver, spleen, lung, jejunum and rectum. Wild rodents, particularly mice, may have been a source of infection for these animals, as the monkeys were housed in a rural, indoor-outdoor facility. A preliminary culture survey showed that some clinically normal patas monkeys harbored the organism in their intestinal tracts.
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PMID:Naturally occurring Yersinia enterocolitica septicemia in patas monkeys (Erythrocebus patas). 405 42

Severe electrolyte disturbances developed after the administration of hypertonic phosphate enemas in 2 chronically obstipated cats. Hyperphosphatemia, hypernatremia, and hypocalcemia were detected in both cats. Physical findings included weakness, anxiety, tachycardia, hypothermia, and dehydration. Intravenous fluid and electrolyte therapy led to prompt, dramatic improvement in both cats. Although well tolerated by most healthy animals, hypertonic phosphate enemas should be avoided in small animals, especially those that are dehydrated, severely obstipated, or suffering from renal or colonic disease.
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PMID:Electrolyte abnormalities induced by hypertonic phosphate enemas in two cats. 408 55

A ferret with clinical and laboratory signs of hypoglycemia was found at surgery to have a beta cell tumor of the pancreas. There had been recurrent episodes of weakness, ataxia, dehydration, and hypothermia. A fasting blood glucose content was 43 mg/dl and the amended insulin/glucose ratio was 362.5. The tumor was removed, yet hypoglycemia persisted postoperatively. Clinical signs related to hypoglycemia did not recur following application of medical treatment and frequent feedings. The histologic appearance of the tumor closely resembles that which has been seen in other species.
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PMID:Pancreatic beta cell tumor in a ferret. 609 38

The effects of body temperature and behavior of 2,4-dinitrophenol injected into the cerebral ventricles of the cat was investigated in these experiments. Infused in a volume of 0.1-0.2 ml, 2,4-dinitrophenol produced a dose-dependent fall in body temperature, the duration of which was also dose-dependent. Apart from hypothermia, 2,4-dinitrophenol evoked mydriasis, respiratory irregularities, urination, vomiting, ataxia, muscular weakness, sedation and occasional clonic-tonic convulsions. Of all the autonomic effects, the most consistent was the effect on thermoregulation. The possible mechanisms of action in the brain of 2,4-dinitrophenol on the thermoregulatory mechanisms are discussed.
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PMID:Hypothermic effect of 2,4-dinitrophenol infused ICV in the cat. 649 41

Adequate nutrition in the severely burned child often determines the morbidity and mortality and its supervision demands a high priority in the management of the burn injury. A disciplined, detailed programme is required, but this is often neglected. The hypermetabolism experienced in the severe burn may require a calorie intake up to 2 1/2 times normal, and in the growing child, with extra requirements, a negative balance can easily eventuate if careful management is not instituted. A daily metabolic plan provides firstly, the basic calories and protein per kilogram depending on age as for a normal child and, secondly additional requirements depending on the surface area of the burn. With such a programme the weakness of treating all children, whatever their age, on the same formula related only to surface area burn, is overcome. Parenteral nutrition is commenced as soon as the shock phase has been controlled and is continued until enteral intake by gastric tube is sufficient to cover the requirements. Such tube feeding requires the selection of an isotonic liquid diet so as so limit the possibility of diarrhoea. Isocal (Mead Johnson) has been found generally acceptable. Gradually as the patient recovers, oral intake is introduced and the child returns home on a normal nutritional diet, expectantly without weight loss and even with some weight gain, which befits any normal child under treatment for some months. Preburn nutrition, disease and infection, hyperthermia, hypothermia, evaporative water loss, active exercise, psychological well being, social state, early skin cover and limitation of stress are important aspects affecting metabolism and require careful supervision and management. The limitation of metabolism is as important as increasing the caloric intake and this is exemplified at the time of operation, which should be as nonstressful as possible. Every two weeks an adjusted assessment is made of the burned area still to be grafted and the caloric requirements are reduced accordingly. Assessment as to the success of the regime is made upon the results of daily weighing. Extra vitamins and elements are given and blood electrolytes and urine glucose and protein are regularly monitored.
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PMID:Nutrition in the severely burned child. 678 87


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