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

The effect of forced cooling was studied as applied to the contents of ammonia, glutamine, glutaminic, asparaginic and alpha-amino butyric acids in the brain of sousliks woken-from hibernation. The cooling of the woken sousliks to the body temperature of 30, 20 and 25 degrees C decreased to some extent the ammonia content in the brain. A deeper hypothermia (10 degrees C) causes its 60,4% decrease as compared to the ammonia amount in woken animals. The cooling of the animals to 30, 25, 20 and 10 degrees C considerably decreases the contents of glutamine, glutaminic acid and GABA in the brain tissue.
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PMID:[Effect of hypothermia on the ammonia-glutamine-glutamic acid system in ground squirrels after hibernation]. 54 34

The content of ammonia, glutamine, dicarboxylic amino acids and GABA was studied in the brain under 1, 2, 4-fold separate and simultaneous effect of hypothermia (19-20 C) and hyperoxia (3 atm.). A two-fold hypothermia of rats is accompanied by a greater increase of ammonia in the brain than a three-fold one. The content of glutamine under two-fold cooling is unchanged and under three-fold cooling it is twice as low as compared to its content in the brain of the control rats. The content of glutamic acid decreased after two-fold hypothermia is almost unchanged by the third seance of hypothermia. The repeated actions of hyperoxia also cause a considerable increase in the ammonia content but the dynamics of changes in the content of the nitrogenous metabolic products is contary to that in animals subjected to repeated seances of hypothermia. A simultaneous combined action of hypothermia and hyperoxia produces no additive effect on the system ammonia-glutaminic acid.
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PMID:[Effect of hypothermia and hyperoxia on the ammonia-glutamic acid system in the brain of rats]. 96 Feb 39

Under various conditions of heating, H35 cells were submitted to acute nutritional deprivation by omitting a number of substrates (L15D medium). At 37 degrees C cell death starts after a lag-period of 3-5 h. During hypothermia cell death is delayed, whereas during hyperthermia it is accelerated especially as a result of thermosensitization. In L15D the ATP level decreases approximately 3 times faster in combination with hyperthermia than at 37 degrees C. In non-thermotolerant cells thermosensization is very high at 41 degrees C and decreases with increasing temperature; in thermotolerant cells it is comparatively decreased at 41 degrees C and increased at 42.5 degrees C and above. In response to a heat shock of 30 min at 42.5 degrees C only 10% of the cell population expresses acute thermotolerance after incubation at 37 degrees C in L15D as compared to nearly 100% in complete medium (L15C). Chronic development of thermotolerance appears to be even more repressed in the presence of L15D, which partly explains the high thermosensitization at 41 degrees C. Changes in the rate of protein synthesis for combinations of nutritional deprivation and hyperthermia show a correlation with the cell survival data. Development of acute thermotolerance in L15D is accompanied by an increase in heat-shock protein synthesis relative to total protein. At 41 degrees C in L15D no heat-shock protein induction could be detected. Of the omitted substrates only glutamine can effectively abolish thermosensitization and the effects of L15D on protein and heat-shock protein synthesis depending on the condition of the cells, thermotolerant or non-thermotolerant, and to a different extent for the various proteins considered.
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PMID:Induction of thermotolerance and heat-shock protein synthesis during nutritional deprivation. 160 42

The effect of hypoxia, cold and hypoxic-cold stress was studied on plasma and brain amino acid levels of rats. Hypoxia caused a considerable increase in plasma taurine and phosphoserine levels, while the remaining amino acids (except valine, cystine, iso-leucine, leucine and anserine) decreased significantly. On the other hand cold stress significantly increased the plasma taurine, asparagine and decreased glutamine, glycine, alanine, methionine and histidine levels. The hypoxic-cold stress combination produced marked decrease in most of the plasma levels of amino acids (except phosphoserine, taurine and anserine). During brain amino acid studies, hypoxia significantly elevated taurine, aspartic acid, valine and leucine levels while the concentrations of other amino acids were not significantly altered. Cold stress was found to elevate taurine and valine levels, while leucine and phenyl-alanine levels were significantly decreased. Exposure of animals to hypoxic-hypothermia affected significantly the brain levels of valine, methionine, leucine and arginine. Since, the change in amino acid levels in brain is less prominent, as compared with plasma, in response to stress, it appeared that brain possesses higher adaptive mechanisms to counteract the stress induced amino acid level imbalance.
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PMID:Effect of hypoxia and/or cold stress on plasma and brain amino acids in rat. 274 Jun 20

Results are reported of a comparative study in vivo of the metabolism of [2-(14)C]-glucose and [1-(14)C]acetate in brains of rats intoxicated with triethyltin sulphate. The incorporation of (14)C from glucose into glutamate, glutamine, gamma-aminobutyrate and aspartate was greatly decreased. The incorporation of (14)C from acetate into these amino acids was unaffected. The experimental data indicated that the main action of triethyltin was to decrease the rate at which pyruvate formed from glucose is oxidized. Glycolysis was not inhibited. Changes in glucose metabolism in the brain are shown not to be directly due to hypothermia. Some of the advantages of measuring the labelling of intermediates at very short time intervals after the injection of the labelled glucose are demonstrated.
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PMID:Selective inhibition of glucose oxidation by triethyltin in rat brain in vivo. 548 56

1. Hypothermia in midwinter revealed a marked increase in GABA and glutamine due to active decarboxylation and amidation of glutamic acid. This influenced the glutamate-aspartate pathway and resulted in a significant drop in levels of both acids. 2. Elevated levels of GABA and taurine during hibernation pointed to their role as inhibitory neurotransmitters. 3. Amidation of glutamate induced a noticeable drop in ammonia concurring with increased urea and low uric acid levels. 4. Hypothermia in summer revealed a significant role of temperature as a determining factor in the hibernation cycle. Arousal was a repeated, though reversed, phenomenon in this cycle.
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PMID:Hibernation hypothermia and metabolism in hedgehogs--changes in free amino acids and related compounds. 612 98

During brain ischemia in vivo the extracellular concentration of the excitotoxic amino acid, glutamate, increases. This increase could be caused either by an enhanced formation rate of glutamate (from glutamine) or by an impaired re-uptake (or both). This re-uptake occurs to a large extent in astrocytes. In the present study we have determined glutamate uptake and the ability of the cells to maintain their glutamate content during exposure to anoxia, substrate deprivation and combined substrate deprivation and anoxia ('simulated ischemia') for a duration of up to 4 h. Isolated anoxia had no significant effect, whereas both substrate deprivation alone and 'simulated ischemia' reduced glutamate uptake and glutamate content by one-half after 2 h. Under hypothermic conditions (incubation at 32 degrees C), which in in vivo experiments exerts some protection against ischemic cell death in neurons, ischemia of intermediate duration (2 h) decreased glutamate uptake and glutamate content to a less extent than at 37 degrees C. Hypothermia did not have a similar effect during exposure to isolated substrate deprivation.
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PMID:Glutamate uptake and glutamate content in primary cultures of mouse astrocytes during anoxia, substrate deprivation and simulated ischemia under normothermic and hypothermic conditions. 810 87

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

Hypothermia has been reported to be beneficial in CNS physical injury and ischemia. We previously reported that posttraumatic cooling to 17 degrees C for 2 h increased survival of mouse spinal cord (SC) neurons subjected to physical injury (dendrite transection) but that cooling below 17 degrees C caused a lethal NMDA receptor-linked stress to both lesioned and uninjured neurons. The present study tested whether cooling below 17 degrees C increases extracellular levels of excitatory amino acids (EAA). SC cultures were placed at 10 degrees C or 37 degrees C. Glutamate (Glu) and aspartate (Asp) levels were higher in the medium of the cooled cultures after 0.5 h (23 +/- 4 nM/microgram vs. 4 +/- 1 nM/microgram and 4 +/- 1 nM/microgram vs. 1 +/- 0 nM/microgram, respectively). The concentration of each EAA then declined and reached a plateau at 2-4 h that was still significantly higher than control levels (p < 0.0001, two-factor ANOVA, three cultures per group). Other amino acids (glycine, asparagine, glutamine, serine) showed an opposite pattern, with higher levels in the 37 degrees C group. Both NMDA and non-NMDA antagonists prevented the lethal cold injury. Survival of SC neurons cooled at 10 degrees C for 2 h and rewarmed for 22 h was 58% +/- 25% in the control group, 94% +/- 5% in the CNQX-treated group, 97% +/- 5% in the DAPV-treated group, and 99% +/- 2% in the group treated with both antagonists [p < 0.0006, one factor ANOVA, five cultures (> 120 neurons) per group]. These results show that death of neurons cooled to 10 degrees C is caused by elevated extracellular Glu and Asp and requires activation of both the NMDA and non-NMDA receptor subtypes.
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PMID:The role of excitatory amino acids in hypothermic injury to mammalian spinal cord neurons. 900 66

We evaluated in rats, the effect of moderate hypothermia (30-31 degrees C) on extracellular levels of amino acids, with special emphasis on the excitatory amino acids (EAAs) glutamate and aspartate, lactate and pyruvate, after severe spinal cord compression. A laminectomy of Th7 and Th8 was made. A probe was inserted in a dorsal horn and microdialysis was performed for 1.5 h before and 4 h after applying severe compression for 5 min. Dialysate samples were collected at intervals of 10 min and analyzed by high-performance liquid chromatography. In normothermic (37.5 degrees C) animals there was a several-fold rise of glutamate that peaked in the first 10 min fraction after trauma. Hypothermic animals showed a similar increase after trauma, which was statistically significant until 20 min after injury. The level of glutamate was significantly higher in hypothermic animals from 20 to 70 min after injury, compared with normothermic animals. Aspartate also showed a marked increase following injury. The peak concentration was similar for both groups, whereas recovery was delayed in hypothermic animals. There was no significant difference between the normothermic and hypothermic animals for arginine, taurine, alanine, glutamine, histadine, glycine, threonine, tyrosine, and asparagine. No significant effect of hypothermia on lactate or lactate/pyruvate was noted. However, the mean level of lactate tended to be lower and recovery was quicker in hypothermic animals. The results of the present study suggest that moderate hypothermia does not attenuate extracellular accumulation of EAAs or markedly improve energy metabolism in our model. Instead, our findings raise the possibility that moderate hypothermia prolongs the duration of glutamate receptor overactivation. Since hypothermia effectively attenuates glutamate release in CNS and spinal cord ischemia models our results suggest different mechanisms of extracellular accumulation of EAAs in ischemia and trauma.
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PMID:Effects of moderate hypothermia on extracellular lactic acid and amino acids after severe compression injury of rat spinal cord. 904 12


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