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

It is found that changes induced by moderate hypothermia (30 degrees C) in the brain tissue glutaminase activity and its temperature dependence are not removed after self-heating up to the body temperature of 37 degrees C. Self-heating after deep hypothermia (20 degrees C) causes a considerable increase in the brain tissues glutaminase activity at all studied incubation temperatures (37, 30, 20 and 10 degrees C) as compared to control rats and rats under hypothermia. The increase in the brain tissue glutaminase activity during self-heating of cooled animals may be considered as a compensatory reaction under conditions of a higher utilization of glutamate by the brain.
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PMID:[Glutaminase activity of the brain during metabolic heating after hypothermia]. 682 82

Experiments on rats have shown an important role of hypercapnia in the development of condition of artificial hibernation in combination with influence of hypothermia, hypoxia and hypercapnia. It is proved that the joint action of hypothermia, hypoxia and hypercapnia has induced development of respiratory acidosis and hibernation in animals, while removal of the hypercapnia effect has induced development of acute metabolic acidosis and death of animals. It has been found that animals in the state of artificial hibernation have considerable changes in concentrations of main electrolytes (Na+, K+, Ca+, Mg2+, phosphates, Cl-) and metabolites (NH3, glutamine, urea) in blood as well as in activity of enzymes (glutamaldehydrogenase, glutaminase, arginase) in tissues of the liver and kidneys.
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PMID:[Acid-base equilibrium and nitrogen metabolism in rats in a state of artificial hibernation]. 855 76

Low temperature optimum of the glutaminase activity in synaptosomal fraction of the brain occurs in deep hypothermia, similar phenomenon occurring in hibernation. The optimum depends on the animal body temperature. The data obtained suggest a manifestation of the temperature compensation.
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PMID:[Temperature compensation in homeothermic animals]. 948 75

Epilepsy is a complex, multifactorial disease characterized by spontaneous recurrent seizures and an increased incidence of comorbid conditions such as anxiety, depression, cognitive dysfunction, and sudden unexpected death. About 70 million people worldwide are estimated to suffer from epilepsy, and up to one-third of all people with epilepsy are expected to be refractory to current medications. Development of more effective and specific antiepileptic interventions is therefore requisite. Perturbations in the brain's glutamate-glutamine cycle, such as increased extracellular levels of glutamate, loss of astroglial glutamine synthetase, and changes in glutaminase and glutamate dehydrogenase, are frequently encountered in patients with epilepsy. Hence, manipulations of discrete glutamate-glutamine cycle components may represent novel approaches to treat the disease. The goal of his review is to discuss some of the glutamate-glutamine cycle components that are altered in epilepsy, particularly neurotransmitters and metabolites, enzymes, amino acid transporters, and glutamate receptors. We will also review approaches that potentially could be used in humans to target the glutamate-glutamine cycle. Examples of such approaches are treatment with glutamate receptor blockers, glutamate scavenging, dietary intervention, and hypothermia.
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PMID:The Glutamate-Glutamine Cycle in Epilepsy. 2788 37