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

Changes in the concentration of amino acids and other metabolites were determined in the perfusate during 24 hr of ex vivo hypothermic perfusion of dog kidneys. There was an increase in concentration of most of the amino acids. Two patterns were identified. One showed an increase in concentrations up to 12 hr, and then a leveling off as exemplified by alanine, serine, and glutamate. The other pattern was one of persistent elevation as exemplified by phenylalanine, threonine, and methionine. Glucose, lactate, pyruvate, sodium, potassium, pH, and pO2 were also measured in the perfusate. The results suggest that a degradation of kidney protein may occur during the first 24 hr of perfusion. The levels of other metabolites measured support the fact that glycolysis is responsible for a considerable portion of the total energy production in the kidney under hypothermia.
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PMID:Changes in concentration of amino acids and other metabolites during hypothermic perfusion of the canine kidney. 374 9

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

Rats treated 4 hr previously with 6-aminonicotinamide showed a twenty-four fold increase of [14C]phosphogluconate in the adult brain at 30 min after injection of [U-14C]glucose indicating a blockade of the hexosemonophosphate shunt. There was a significant increase in the 14C-content of glucose and glucose-6-phosphate, and a decrease in that of amino acids. [14C]Phosphoglycerate content showed no consistent change after 6-aminonicotinamide treatment. The concentration of glucose and glucose 6-phosphate increased significantly without a significant change in the lactate pool in the brain of 6-aminonicotinamide treated rats. The rate of utilization of glucose in the brain of control rats was 0.73 mumol/min per g of brain. It decreased by 16% in rats treated with 6-aminonicotinamide; the results suggested that both glycolysis and pyruvate oxidation were affected. The amount of glucose utilized in the brain by the hexosemonophosphate shunt was approximately 0.0093 mumol/min per g of brain, i.e. 1.3% of the total rate of utilization of glucose. The observed changes were not due to hypothermia. The rate of glucose utilization was higher in animals exposed to higher ambient temperature and to stress caused by handling. The results were explained by postulating a role for the hexosemonophosphate shunt in providing neurotransmitter amino acids glutamate and gamma-aminobutyrate, and interdependence of brain function and glucose utilization.
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PMID:The effect of inhibition of hexosemonophosphate shunt on the metabolism of glucose and function in rat brain in vivo. 621 28

A low dose (1 microgram) of intracerebroventricularly injected (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) produced a hyperthermic response in rats, while a high dose of AMPA (2.5 micrograms), similarly to kainic acid (0.1 microgram) produced a biphasic effect: short-lasting hypothermia followed by hyperthermia. These effects on body temperature were not affected by pretreatment with 200 mg/kg ip of glutamic acid diethylester (GDEE), which by itself, produced a significant hypothermia. The results indicate that the effects of kainic acid and AMPA on body temperature are not mediated by GDEE-sensitive glutamate receptors.
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PMID:Effect of glutamic acid diethylester on (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and kainic acid-induced changes of body temperature in rats. 630 Aug 14

Pentobarbital anesthesia has been observed to increase markedly the effectiveness of respiration of oxygen at 3 atmospheres of pressure absolute to increase the response of early generation isotransplants of C3H mouse tumors to two-dose irradiation. A possible mechanism of this phenomenon is suppression of oxygen utilization by the pentobarbital and hence increasing mean pO2 and oxygen diffusion lengths. Measurements of QO2 of suspension of MCaIV and FSaII cells from freshly excised tumor tissue have been measured for cells suspended in PBS, Hank's buffered with HEPES +/- glutamate. The oxygen utilization by these tumor cells in vitro (when measured at congruent to 10 minutes after excision) is low, viz. 1 nmole/min/mg protein as compared with 6-9 nmoles/min/mg protein for established cell lines cultured in vitro. The suppression of QO2 by 2mM pentobarbital is less than 10%. This is a concentration of pentobarbital that is judged to be close to that which obtains in the tissues of the animals in the radiation response assays. Pentobarbital at .2mM did not change the cell survival characteristics of Chinese V79 cell spheroids irradiated in vitro. The results of these experiments do not indicate the suppression of oxygen utilization is an important contributor to the observed phenomenon of the increased response of tumors irradiated in mice respiring oxygen at high pressure. The role of hypothermia produced by the anesthesia is under further study.
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PMID:On the mechanism for enhancement of tumor radiation to hyperbaric oxygen in sodium pentobarbital anesthetized rodents. 653 7

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

Glutamate, dehydrogenase activity and its temperature dependence were studied in the rat brain at moderate (30 degrees C) and deep (20 degrees C) hypothermia. Depending on the grade and duration, hypothermia led to an increase in the enzyme activity at all the test temperatures of incubation. It is assumed that an increase in brain glutamate dehydrogenase activity at low body temperatures favours high level of the neurotransmitter glutamate to realize synaptic transmission, which may be regarded as adaptation reaction.
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PMID:[Effect of hypothermia on glutamate dehydrogenase activity of the brain]. 717 20

In vitro ischemia models have utilized oxygen, or oxygen and glucose deprivation to simulate ischemic neuronal injury. Combined oxygen and glucose deprivation can induce neuronal damage which is in part mediated through NMDA receptors. Severe oxygen deprivation alone however can cause neuronal injury which is not NMDA mediated. We tested the hypothesis that NMDA, or non-NMDA receptor mediated mechanisms may predominate, to induce neuronal injury following severe oxygen deprivation depending on the presence of glucose. We found that NMDA receptor blockade using dizocilpine (MK-801), DL-2-amino-5-phosphonovaleric acid (APV), or CGS 19755, was highly effective in reducing CA1 injury in organotypic hippocampal cultures, caused by complete oxygen and glucose deprivation. Complete oxygen deprivation alone however, caused CA1 neuronal injury which was not diminished using NMDA receptor blockade alone with MK-801 or APV, or in combination with AMPA/kainate receptor blockade using 6-cyano-7-dinitroquinoxalone-2,3-dione (CNQX). Neuronal protective strategies which act primarily through non-glutamate dependent mechanisms, including hypothermia, low chloride and calcium, and the free radical scavenger, alpha-phenyl-tert-butyl nitrone (PBN), provided neuronal protection against complete oxygen, as well as combined oxygen/glucose deprivation. Raising the pH using Hepes buffer during complete oxygen deprivation did not result in neuronal protection by NMDA receptor blockade. Partial oxygen deprivation alone, partial oxygen deprivation combined with glucose deprivation, glucose deprivation alone, and also glutamate exposure, all produced neuronal damage that was reduced by NMDA receptor blockade. The presence of glucose during complete oxygen deprivation appears to prevent glutamate receptor blockade from reducing neuronal injury in organotypic hippocampal cultures.
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PMID:Glutamate and non-glutamate receptor mediated toxicity caused by oxygen and glucose deprivation in organotypic hippocampal cultures. 747 21

We examined the effect of moderate hypothermia (30 degrees C) on neuronal injury in murine cortical cell cultures. Lowering the temperature during and after a period of oxygen-glucose deprivation reduced both the release of glutamate to the bathing medium and accompanying neuronal degeneration. Hypothermia immediately after brief exposure to high concentrations of NMDA or glutamate also reduced the resulting neuronal degeneration. This protective effect was not eliminated when MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione were added immediately after washout of the exogenously added excitotoxin, suggesting that it was mediated by actions additional to reduction of endogenous late glutamate release. Hypothermia applied only during exposure to NMDA or glutamate, whether brief or prolonged, did not reduce subsequent cytosolic calcium accumulation or neuronal degeneration, suggesting that the postsynaptic induction of NMDA receptor-mediated excitotoxicity is not sensitive to temperature reduction. However, hypothermia during prolonged S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or kainate exposure did reduce neuronal degeneration.
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PMID:Neuroprotective effect of hypothermia in cortical cultures exposed to oxygen-glucose deprivation or excitatory amino acids. 752 91


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