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

The temperature dependence of the incorporation of amino acids into cerebral proteins and that of the transport of amino acids through the blood-brain barrier were studied. We measured the protein synthesis rate in vivo over a wide temperature range (14 degrees C-38 degrees C) in male Sprague-Dawley rats using a flooding dose of labeled valine. There was a linear dependence of the protein synthesis rate on temperature. The temperature quotient expressed as per cent decrease per 1 degree C was somewhat lower at the lower temperatures, a decrease from 7.8% in the 37.7-32.5 degrees C range to 6.7% in the 25.5-14 degrees C range. The transport of the three amino acids phenylalanine, lysine, and alanine, representing three transport systems, through the blood-brain barrier showed no temperature dependence in vivo. The results show that in hypothermia cerebral metabolic rates are lowered to a great extent, while some aspects of metabolic transport are not affected.
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PMID:Different effects of hypothermia on amino acid incorporation and on amino acid uptake in the brain in vivo. 160 61

The effects of intracerebroventricularly (icv.) administered oxytocin (OXT) and lysine-8-vasopressin (LVP) on the development of hypothermic tolerance to ethanol were investigated. Mice equipped with an icv cannula were pretreated with graded doses of OXT or LVP (3 ng, 300 pg, 30 pg or 3 pg/animal) before the daily intraperitoneal ethanol (4 g/kg) injection. Two doses of OXT or LVP (3 ng or 300 pg/animal) blocked the development of hypothermic tolerance to ethanol. Smaller doses of the peptides were ineffective in inhibiting the gradual decrease in hypothermia upon repeated ethanol administration, which effect was observed in the control group. The data presented show that the central administration of these neurohypophyseal peptides blocks the development of tolerance to ethanol.
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PMID:Intraventricular administration of neurohypophyseal hormones interferes with the development of tolerance to ethanol. 271 43

Pipecolic acid (PA) is an intermediate of lysine metabolism in the mammalian brain. Recent findings suggest a functional connection of PA as neuromodulator in GABAergic transmission. Since many drugs are postulated to produce their effects by interaction with the central GABA system, the influence of PA on the anticonvulsant activity of phenobarbital was examined. Pretreatment of mice with 50 mg . kg-1 of PA potentiated the suppressing effects of the barbiturate on electrically and chemically induced convulsions. However, there was no potentiation of the behavioral effects and hypothermia induced by phenobarbital. PA itself had no or only little effect on the convulsions, motor function and rectal temperature when given in i.p. doses up to 500 mg . kg-1. Intraventricular administration of 500 microgram of PA also did not suppress either type of convulsion, although it produced ptosis, hypotonia, sedation and hypothermia. The results are discussed in relation to GABA system.
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PMID:Potentiation of phenobarbital-induced anticonvulsant activity by pipecolic acid. 628 9

The effects of centrally injected prostaglandins (PGE1 and PGF2 alpha), arachidonic acid and lysine acetylsalicylate were examined on the seizure activity and temperature changes produced by pentylentetrazole (PTZ) and also on maximal electroshock (MES) seizures. PGE1 antagonised both PTZ and MES seizures whilst PGF2 alpha had the reverse effect. In addition both PGs alone produced hyperthermia but attenuated PTZ hypothermia. Arachidonic acid protected against PTZ--but potentiated MES--seizures whilst lysine acetylsalicylate augmented the effects of both convulsive stimuli. Lysine acetylsalicylate and arachidonic acid alone were transiently hyperthermic and also antagonised PTZ hypothermia though the total net effect may have been due to a functional antagonism. It is suggested from these findings that PGE1 has anticonvulsant effects whilst PGF2 alpha promotes seizures neither of these properties correlating with thermoregulatory actions.
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PMID:Modification of convulsive behaviour and body temperature in mice by intracerebroventricular administration of prostaglandins, arachidonic acid and the soluble acetylsalicylic acid salt lysine acetylsalicylate. 679 2

The neurohypophyseal hormone, arginine vasopressin (AVP), was previously shown to prolong the duration of ethanol tolerance in mice. Since drug tolerance and certain memory-related processes are examples of CNS adaptation, these phenomena have been proposed to share underlying mechanisms. We investigated the effects on ethanol tolerance of two other neurohypophyseal peptides, both of which modulate memory consolidation or retrieval of information. (Des-9-glycinamide, 8-lysine) vasopressin (DGLVP), like AVP, maintained ethanol tolerance in C57Bl mice, while cyclo(Leu-Gly) (cLG), at an equimolar dose, was ineffective. Thus, various neurohypophyseal peptides may differentially influence CNS adaptive phenomena. Direct peptide effects on ethanol-induced hypothermia and "sleep time," the parameters used to evaluate ethanol tolerance, were also determined. AVP per se caused hypothermia in mice, but neither AVP nor cLG affected ethanol-induced hypothermia. Both peptides, however, increased "sleep time" after acute ethanol administration. Although these direct peptide-ethanol interactions do not account for the observed peptide effects on tolerance, the findings emphasize the importance of using several parameters to assess ethanol tolerance.
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PMID:Neurohypophyseal peptide influences on ethanol tolerance and acute effects of ethanol. 724 29

Protamine sulfate is routinely administered after cardiopulmonary bypass to reverse systemic heparinization, but may cause a severe hypotensive reaction in as many as 2% of patients. Research Medical, Inc., has developed an extracorporeal venovenous heparin removal device (HRD) for use in patients at high risk for a protamine reaction. Circulation through the HRD removes heparin by hollow fiber plasma separation and selective sorption of anionically charged heparin to a polycationically charged poly-L-lysine ligand coupled to a agarose substrate. The heparin depleted plasma then reenters the whole blood pathway and is returned to the patient through the double lumen catheter in the right atrium. To evaluate the HRD in a clinically relevant model, cardiopulmonary bypass was performed in pigs using RA-Ao cardiopulmonary bypass (120 min) with systemic heparinization (300 IU/kg), a nonpulsatile pump with a membrane oxygenator, and systemic hypothermia (28 degrees C). Group 1 (HEP n = 7) had no intervention to neutralize the heparin; Group 2 (HRD n = 7) used the HRD. After 19.7 +/- 4.2 min of circulation through the HRD, the activated clotting time had returned to baseline, whereas the pigs in the HEP group were still anticoagulated (activated clotting time = 396 +/- 152 sec; time to baseline was 124 +/- 9 min). There were no significant differences between groups with respect to hemodynamics, hematocrit levels, leukocyte profiles, or platelet counts, HRD is an effective heparin removal device in a pig model of cardiopulmonary bypass and awaits a phase I clinical trial in humans.
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PMID:Reversal of anticoagulation without protamine using a heparin removal device after cardiopulmonary bypass. 855 77

Cold preservation of kidneys is commonly used in human transplantation and in vitro studies. However, although disruption of the cytoskeleton by cold has been demonstrated in cultured cells, the effect of cold treatment on intact kidney is poorly understood. In this study, specific antibodies were used to examine the effect of hypothermia on the cytoskeletal network and the trafficking of some membrane proteins in the urinary tubule. Rat kidneys were cut into thin slices (approximately 0.5 mm) that were divided into several groups: (1) some were immediately fixed in paraformaldehyde, sodium periodate, and lysine (PLP); (2) some were stored at 4 degrees C for 15 min or 4 h before being fixed in cold PLP; or (3) after 4 h cold treatment, some slices were rewarmed to 37 degrees C for 15, 30, and 60 min in a physiologic solution, pH 7.4, and were then fixed in warm PLP. Immunofluorescence staining revealed an almost complete disruption of the microtubule network in proximal tubules after 15 min cold treatment, whereas microtubules in other segments were affected after 4 h. A partial recovery of the microtubule network was observed after 60 min rewarming. In contrast, actin filaments seemed to be resistant to cold treatment. gp330, aquaporin-2, H+ ATPase, and the AE1 anion exchanger were all relocated into numerous vesicles that were distributed throughout the cytoplasm after hypothermia followed by rewarming, whereas Na-K-ATPase retained its basolateral localization. The vasopressin-stimulated insertion of aquaporin-2 water channels into the apical membrane was inhibited during the initial rewarming period after cold exposure. Thus, cold preservation of tissues might impair, at least transiently, the polarized membrane expression and function of some transport proteins in renal epithelial cells.
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PMID:Cold-induced microtubule disruption and relocalization of membrane proteins in kidney epithelial cells. 952 91

Investigations into cardiopulmonary bypass continue to refine knowledge and clinical practice. Recent investigations have emphasized neurological complications, introducing the possibility of genetic predisposition as a risk factor. Appropriate flows, pressures, and hematocrit levels during cardiopulmonary bypass continue to create controversy. Whereas previous debate has centered around appropriate temperature management, recent discussions consider the possibility that mild hypothermia after cardiopulmonary bypass might be neuroprotective. Meta-analyses and prospective investigations continue to suggest the virtual equivalence of aprotinin and lysine analogues in reducing bleeding and transfusion after cardiopulmonary bypass. Several recent studies identified the mechanisms and severity of the inflammatory response to cardiopulmonary bypass, as well as possible techniques for attenuating inflammation.
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PMID:Update on cardiopulmonary bypass. 1701 78

Effect of an autumn-winter decrease of the environmental temperature on changes of the content of free amino acids and reducing sugars was studied in tissue fluids of the freshwater mollusc L. stagnalis. At a decrease of the temperature to 4 and 0 degrees C at the autumn period, concentration of free alanine rose several times; an increase of histidine, glutamate, glycine, and serine concentrations was less pronounced. Accumulation of methionine, leucine, isoleucine, tyrosine, and phenylalanine was revealed at 0 degree C. In the state of long hypobiosis (at 4 degrees C), pools of all amino acids fell 4-8 times; essential amino acids, except for lysine, were not detected at all. Both at the summer and at the autumn periods, high concentrations of free fructose and glucose were revealed. In the process of hypobiosis the fructose pool decreased almost 35, while the glucose pool--12 times. Maltose that was absent in summer was found at 4 and 0 degree C as well as after 2.5 months of hypobiosis. The changes of the studied parameters in L. stagnalis in response to hypothermia are compared with the corresponding parameters of changes in cryoresistant animals in response to negative temperatures.
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PMID:[Biochemical strategy of survival of the freshwater mollusc Lymnaea stagnalis at near-zero temperatures]. 1772 30

Histone H3 lysine 9 (H3K9) methylation is a crucial epigenetic mark of heterochromatin formation and transcriptional silencing. Recent studies demonstrated that most covalent histone lysine modifications are reversible and the jumonji C (JmjC)-domain-containing proteins have been shown to possess such demethylase activities. However, there is little information available on the biological roles of histone lysine demethylation in intact animal model systems. JHDM2A (JmjC-domain-containing histone demethylase 2A, also known as JMJD1A) catalyses removal of H3K9 mono- and dimethylation through iron and alpha-ketoglutarate dependent oxidative reactions. Here, we demonstrate that JHDM2a also regulates metabolic genes related to energy homeostasis including anti-adipogenesis, regulation of fat storage, glucose transport and type 2 diabetes. Mice deficient in JHDM2a (JHDM2a-/-) develop adult onset obesity, hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia and hyperleptinemia, which are hallmarks of metabolic syndrome. JHDM2a-/- mice furthermore exhibit fasted induced hypothermia indicating reduced energy expenditure and also have a higher respiratory quotient indicating less fat utilization for energy production. These observations may explain the obesity phenotype in these mice. Thus, H3K9 demethylase JHDM2a is a crucial regulator of genes involved in energy expenditure and fat storage, which suggests it is a previously unrecognized key regulator of obesity and metabolic syndrome.
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PMID:Obesity and metabolic syndrome in histone demethylase JHDM2a-deficient mice. 1962 51


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