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

The ability of chronic ethanol treatment to alter CNS membrane lipids was tested. Adult C57/BL6 mice were given a liquid diet containing ethanol for eight days. This regimen produced strong physical dependence as judged by withdrawal seizures, tremors and concomitant hypothermia. Analyses were performed on cholesterol, total phospholipid content and total phospholipid acyl composition of myelin, crude (P2), light and heavy synaptosomes as well as synaptosomal plasma membranes. Chronic ethanol treatment had no effect on total phospholipid levels nor phospholipid acyl composition in any of the above subcellular fractions. In ethanol dependent mice, significant increases in cholesterol content and cholesterol/phospholipid ratios were observed in synaptosomal plasma membranes.
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PMID:Alterations in brain lipid composition of mice made physically dependent to ethanol. 689 Jun 13

The authors carried out studies on the preparation menilon in order to establish eventual correlations between some pharmacological and pharmakokinetic indices. For this purpose they examined the activity of menilon in rats and mice during electric shock and hypothermia and determined the concentrations of the preparation in plasma and brain in rats. The obtained results from the pharmacological investigation revealed manifested action against the seizures after electric shock in both groups of animals. It was established as early as 30 minutes after oral administration of the preparation reached maximal activity after 1-2 hours and disappeared after 6 hours. The authors found strong and continuous hypothermic activity. The hypothermic effect of the doses used was preserved up to the end the 24 th hour. The lowering of temperature in rats was comparatively weaker and shorter. The pharmacokinetic studies showed quick oral resportion of menilon. It was found in plasma and brain of the experimental animals on the 30 th minite after its administration, reached maximal concentration between the first and second hour and still was established on the 24 th hour after administration. The maximal level of the preparation in plasma and brain after oral administration correlated well with the time of maximal activity of its antiseizure and hypothermic effects. The preparation menilon was comparatively slightly toxic.
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PMID:[Correlations between the pharmacological effects of menilon and its concentrations in the plasma and brain of experimental animals]. 689 34

The behavioral and physiological effects of L-phenylisopropyladenosine, cyclohexyladenosine and 2-chloroadenosine were examined in mice and rats. These analogs of adenosine are agonists which bind with high affinity to putative central A1 receptors in vitro. Relatively low doses of these drugs administered i.p. produced marked sedation and hypothermia; higher doses resulted in an almost complete cessation of spontaneous motor activity as well as some ataxia. These analogs also antagonized seizures elicited by a variety of convulsants with different mechanisms of action. The differences observed in the anticonvulsant potencies of the analogs suggest that these effects are not produced by the interaction of these drugs with a single class of adenosine receptor. In particular, 2-chloroadenosine and cyclohexyladenosine appear to be more related to each other pharmacologically than to L-phenylisopropyladenosine. Because some of the anticonvulsant actions of L-phenylisopropyladenosine are not reversed by the adenosine antagonist theophylline, and are not shared by the other analogs, these may reflect actions mediated by other, perhaps nonpurinergic receptors. Although benzodiazepines also have sedative, hypothermic and anticonvulsant properties, responses to benzodiazepines can be clearly dissociated from responses to the adenosine agonists.
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PMID:Sedative and anticonvulsant effects of adenosine analogs in mouse and rat. 705 24

We studied 2 of 4 affected boys with a new disease associated with abnormalities of copper metabolism. The four cases occurred in two generations of a family. This syndrome was similar to Menkes disease in some respects: X-linked recessive inheritance, marked psychomotor retardation with seizures, low serum copper and ceruloplasmin levels, and a block in gut copper absorption. There were also striking differences from Menkes disease. Patients had normal birthweight at term, no hypothermia, and survived beyond the usual Menkes age group with static neurologic disease including hypotonia and choreoathetosis. In addition, general examination of both children was unremarkable apart from undescended testes and growth retardation. The hair, facies, and skin were normal and there was no radiologic evidence of bony changes. Detailed studies of copper absorption were performed.
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PMID:An X-linked disease of the nervous system with disordered copper metabolism and features differing from Menkes disease. 719 7

Chronic exposure to phenobarbital at a 21-22 degrees C ambient temperature produced marked hypothermia in C57BL/6J male mice, to which functional tolerance gradually developed over a 6.5 day intoxication period. Soon after phenobarbital withdrawal, marked hypothermia again developed, reaching its maximal extent at a time when tremors, convulsions on handling and Straub tail were at their peak frequency. When these mice were placed in a 34 degrees C ambient environment, which prevents the hypothermia, these withdrawal signs were eliminated or greatly reduced in frequency compared to mice at 22 degrees C, whereas the incidence of tonic-clonic seizures was not significantly affected. Core body temperature was found to correlate significantly with the degree of gross intoxication during the intoxication phase and with the withdrawal signs of tremor and Straub tail after withdrawal of the drug. When mice were given a choice between a 23 and a 35 degrees C environment at times of maximal hypothermia, their choice often served to maintain the hypothermic state rather than to reduce it. These results suggest that some of the signs of withdrawal (tremor and Straub tail) may be (in part) secondary responses to a primary dysfunction, which is thermoregulatory in nature.
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PMID:Barbiturate physical dependence in mice: effects on body temperature regulation. 719 49

Trimethyltin (TMT) chloride, administered to adult male Long-Evans hooded rats, produced a unique and distinctive behavioral syndrome consisting of spontaneous seizures, tail mutilation, vocalization and hyperreactivity. The LD50 for TMT was weight dependent; in large rats (e.g., 450 g), 7 mg/kg TMT produced significant weight loss and lethality, whereas in small rats (e.g., 250 g), 7 mg/kg produced neither weight loss nor lethality. TMT produced mild hypothermia and tremors. Results are discussed in comparison with kainic acid-induced morphological alterations and septal lesion-induced behavioral alterations. Histopathological evaluations of hippocampal tissue revealed cell loss that was largely confined to regio inferior pyramidal cells. TMT offers potential as a tool for investigations of limbic system structure and function.
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PMID:The trimethyltin syndrome in rats. 720 Oct 84

The author reviewed records of 10 patients who had experienced acute loxapine overdose. The most frequent medical complications were CNS depression, sinus tachycardia, hypertension, and hypothermia; 6 patients had had generalized major motor seizures, 1 had had recurrent paroxysmal atrial tachycardia, and 2 had had transient renal insufficiency from rhabdomyolysis and myoglobinuria. Other clinical effects from loxapine overdose were predominantly anticholinergic. The author recommends that loxapine-overdose patients receive ECG monitoring and treatment of medical complications in an intensive care unit.
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PMID:Seizures induced by acute loxapine overdose. 725 88

The effects of lidocaine in high doses, i.e. higher than seizure doses, on cerebral function and metabolism are reviewed. Evidence is presented that lidocaine (160 mg/kg) reduces membrane NA+-K+ permeability, restricts leak fluxes of these ions, and decreases the load on the associated ion transport. In the ischemic brain (circulatory arrest in dogs on cardiopulmonary bypass circulation), lidocaine delays K+ efflux, indicating reduced membrane permeability. In the nonischemic brain lidocaine has two effects. One is to abolish electrocortical activity and reduce oxygen and glucose consumption accordingly ("barbiturate-like" effect). The other is a specific membrane sealing effect by which Na+-K+ leak fluxes are restricted and associated demand for active transport according reduced. By this effect lidocaine is able to reduce cerebral metabolism by an additional 15-20% below the barbiturate minimum at flat EEG. These effects of lidocaine resemble those of hypothermia and may enhance the hypothermic protection of the ischemic brain.
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PMID:Inhibition of cerebral metabolism by lidocaine. 726 21

Eight infants, 2 to 5 months of age, who were seen somnolence or irritability, seizures, and hypothermia are described. The symptoms developed following the ingestion of dilute formula. All infants were hyponatremic. Three patients were identified by the symptom complex and were evaluated prior to any therapeutic intervention. Plasma arginine vasopressin concentration and urinary osmolality were either normal or increased despite hyponatremia and decreased serum osmolality. These data, coupled with rapid biochemical and clinical improvement following fluid restriction and/or administration of 3% NaCl, strongly implicate the excessive release of arginine vasopressin in the pathogenesis of this syndrome of water intoxication.
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PMID:Water intoxication in normal infants: role of antidiuretic hormone in pathogenesis. 727 59

The requirement of greater than one minute of positive pressure ventilation was prospectively used to identify infants suffering from asphyxia at birth in 38,405 consecutive deliveries. Multivariate analysis of high-risk factors associated with increased risk of asphyxia showed the prematurity was the most significant predictor of asphyxia. Asphyxia occurred in 62.3% of infants less than 27 weeks' gestation and decreased to 0.4% in infants greater than 38 weeks' gestation. Presence of asphyxia was associated with significant increase in neonatal mortality of infants greater than 36 weeks' gestation. Of the asphyxiated neonates, growth retardation, hypothermia, hyaline membrane disease, and seizures were significantly associated with an increased risk of death.
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PMID:Neonatal asphyxia. I. Relationship of obstetric and neonatal complications to neonatal mortality in 38,405 consecutive deliveries. 736 99


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