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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 2-deoxy-D-glucose on lipolytic processes in the blood and adipose tissue was studied. Rats treated with this antimetabolite showed a significant increase in serum glucose, FFA and glycerol level, as well as in the lipid mobilizing activity. On the other hand, the lipolytic activity of rat serum decreased when compared to control group. From these results it may be concluded that during hypothermia induced by administration of 2-deoxy-D-glucose intracellular, but not intravascular, lipolysis is enhanced.
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PMID:Effect of 2-deoxy-D-glucose on lipolytic processes in blood and adipose tissue of rat. 383 83

Hypothermia may be associated with compromised host defenses and serious bacterial infections in man. We have examined the effects of moderate hypothermia (29 degrees C) on neutrophil function in vitro. At 29 degrees C, neutrophil phagocytosis of Staphylococcus aureus was impaired. In contrast, neutrophil killing of Streptococcus faecalis was most affected by hypothermia. Phagocytosis, as measured by neutrophil ingestion of opsonized oil-red-O-particles, was reduced at 29 degrees C over the 15 min of observation. Neutrophil metabolism linked to bactericidal pathways dependent on oxidative metabolism was reduced at 29 degrees C. Hexose monophosphate pathway (HMP) activity in neutrophils early after stimulation with latex particles was reduced. After 2 hr HMP activity was similar at 29 degrees C and 37 degrees C. Neotetrazolium dye reduction was reduced early after latex stimulation of neutrophils and after 30 min it was similar to cells at 37 degrees C. Leukocyte migration under agarose to bacterial-derived and formyl-methionyl-phenylalanine chemotactic factors was reduced by 50% and 70%, respectively. Migration to serum-derived chemotactic factor was reduced by only 20%. When cells were cooled to 29 degrees C for 30 to 90 min and rewarmed, neutrophil function was normal. These effects of hypothermia on neutrophil function may explain, in part, the increased incidence of serious and frequently fatal bacterial infections in man.
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PMID:The effects of hypothermia on neutrophil function in vitro. 391 85

Glucoprivic stress induced by 2-DG (2-deoxy-D-glucose) is associated with increased oxygen consumption (thermogenesis) and sympathetic nervous system activity, as well as elevations of circulating levels of various hormones and metabolic substrates. To examine the role of beta-adrenergic stimulation in the thermogenic, hyperglycemic, and lipolytic responses to glucoprivation, we administered intravenous infusions of propranolol or normal saline (placebo) during 2-DG challenges in seven healthy males. 2-DG alone produced large increments in plasma catecholamine levels, hyperglycemia, a 3.5-fold increase in plasma free fatty acid (FFA) levels, a 15 beat/min increase in pulse rate, and hypothermia in spite of a 20% increase in oxygen consumption. When propranolol was given, 2-DG produced only a 50% increase in FFA levels, no change in oxygen consumption, and a 17 beat/min fall in pulse rate associated with a 25% increase in mean arterial blood pressure. Propranolol only slightly attenuated the hyperglycemia and hypothermia associated with 2-DG but potentiated the elevations of plasma epinephrine levels. It is concluded that 2-DG-induced thermogenesis and lipolysis are primarily dependent on beta-adrenergic stimulation.
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PMID:Beta-adrenergic blockade inhibits thermogenesis and lipolysis during glucoprivation in humans. 612 26

Opioid peptides may act as neuromodulators in the central nervous system to conserve energy stores and water in mammals. To examine this hypothesis in man, the effect of opiate receptor blockade with naloxone on the hunger, thirst, and hypothermic response to 2-deoxy-D-glucose-induced glucoprivic stress was assessed. Opiate receptor blockade decreased stress-induced food intake but did not reduce marked increases in hunger produced by glucoprivation. Naloxone infusions did not change the hypercortisolemic, polydipsic, hypothermic, and thermogenic response to 2-deoxy-D-glucose. While these results do not suggest a major role for a beta-endorphin modulation of stress-induced hunger, hypothermia and water conservation, the reduction of food intake could be due to augmented satiety, perhaps associated with retardation of gastric emptying during opiate receptor blockade.
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PMID:Opiate receptor blockade in man reduces 2-deoxy-D-glucose-induced food intake but not hunger, thirst, and hypothermia. 629 33

During hypothermia induced by intraperitoneal administration of 2-deoxy-D-glucose (600 mg/kg of body weight) the serum levels of glucose and FFA rise and the hepatic glycogen content falls in relation to rats in control group. The glycogenolytic activity of the serum in vitro determined against liver slices is also higher in the group of rats receiving 2-DG. The obtained results point to an activation of the glycogenolysis process and glycolysis in the organism of rats after administration of hypothermia-inducing doses of 2-DG.
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PMID:In vitro serum glycogenolytic activity in rats during hypothermia induced with 2-deoxy-D-glucose. 653 17

Capsaicin modulates animal pain perception, increasing chemosensitive and pressure thresholds following systemic administration, increasing thermal thresholds following intrathecal administration, and decreasing electric shock thresholds following intracerebroventicular (ICV) administration. Since morphine analgesia is decreased in a dose-dependent manner following ICV capsaicin, the present study examined whether ICV injections of capsaicin (0, 25, 50, 100 micrograms) would alter other analgesic responses as well. Experiment 1 demonstrated that the analgesic response to a 450 mg/kg dose of 2-deoxy-D-glucose was significantly reduced by the 25 and 50, but not the 100 micrograms capsaicin dose. Further, while analgesia induced by cold-water swims (CWS) in a 2 degrees C bath was significantly attenuated by the 25 micrograms capsaicin dose, the entire dose range eliminated analgesia induced by CWS in a 15 degrees C bath. Experiment 2 indicated that the capsaicin-induced alterations in CWS analgesia were not attributable to parallel changes in CWS hypothermia. Experiment 3 demonstrated that capsaicin failed to alter both the non-opioid analgesic response induced by 20 inescapable foot shocks (FS) and the opioid analgesic response induced by 80 FS. These data are discussed in terms of the similarities to and/or dissimilarities from capsaicin-induced effects upon morphine analgesia.
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PMID:Capsaicin treatment and stress-induced analgesia. 668 8

Hypothermia in humans during insulin-induced glucopenia has been largely attributed to impaired heat production. To further study the mechanism for hypothermia during glucoprivation six normal males were given 20-min intravenous infusions of 2-deoxy-D-glucose (2-DG), 50 mg/kg, a competitive inhibitor of glucose utilization. Oxygen and carbon dioxide exchange was measured to determine heat production by indirect calorimetry. Decreases in core temperature were initially associated with activation of mechanisms for heat loss such as sweating and hyperpnea 30-120 min after 2-DG infusion. Hypothermia persisted in spite of markedly increased plasma catecholamine, glucose, and free fatty acid levels from 60 to 180 min and increased heat production from 120 to 180 min after 2-DG infusion. Thus in contrast to the proposed mechanism for insulin-induced hypothermia, the hypothermia of 2-DG-induced glucoprivation is a consequence of increased heat loss and not of decreased heat production.
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PMID:Thermoregulatory and related responses to 2-deoxy-D-glucose administration in humans. 677 17

Four critically injured children receiving large doses of phenobarbitone were studied during hypothermia (30 degrees - 31 degrees C) and at normal body temperature. The volume of distribution of phenobarbitone varied from 0.79 to 1.01 litres per kg and the serum t 1/2 ranged from 36.8 +/- 9.4 to 86.2 +/- 10.5 hrs. The percentage of dose recovered in urine in 16 days ranged from 40.5 to 65.5 per cent: 2.7 to 12.4 per cent as hydroxyphenobarbitone, 1.7 to 19.7 per cent as conjugated hydroxyphenobarbitone, 6.0 to 22.4 per cent as phenobarbitone-N-glucoside and 17.8 to 23.1 per cent as unchanged drug. After the body temperature was allowed to return to normal the rate of excretion of metabolites increased substantially and the rate of excretion of the unchanged drug decreased markedly. It is concluded that reduction in body temperature influences the volume of distribution, rate of metabolism and excretion of phenobarbitone.
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PMID:The fate of phenobarbitone in children in hypothermia and at normal body temperature. 705 40

The hypothesis tested was that the composition of the prime and the perfusate at the time of reperfusion had an influence on postischemic cardiac performance. Twelve dogs in two equal groups had long (210 +/- 10 minutes) hypothermic (25 degrees +/- 1 degree C) perfusions. Each had 180 minutes of global ischemia and were given 500 ml of the same cold (4 degrees C) cardioplegic solution (CPS) every 45 minutes and topical hypothermia with a resultant average myocardial temperature of 10 degrees +/- 2 degrees C. Group A had a prime (1,958 ml) consisting of a 50/50 mixture of 5% dextrose in water and 5% dextrose in Ringer's injection to which mannitol (12.5 gm), furosemide (20 mg), and heparin (6,000 units) were added. Group B received a prime (1,868 ml) of 5% dextrose in Ringer's injection (1 L) and 750 ml of 6% helastarch in normal saline to which NaHCO3 (10 mEq), furosemide (20 mg), mannitol (25 gm), and heparin (6,000 units) were added. During perfusion, Group A received lactated Ringer's solution and Group B received a 1 : 2 portions of Ringer's injection and 6% helastarch. Additionally, Group B received additional furosemide and mannitol 5 minutes prior to the reperfusion interval. The results showed a marked difference between groups in postischemic cardiac recovery 120 minutes after cessation of cardiopulmonary bypass. The Group B dogs had statistically (less than 0.02) greater cardiac output, stroke volumes, and stroke work index at equal preloads and lower total peripheral resistances. Arterial systolic, diastolic, and mean pressures and right atrial pressures were not different. The Group A dogs required nearly threefold the volume of fluid additions required during bypass and twice the amount of NaHCO3 as Group B dogs. It is concluded that the composition of the prime and fluids used during bypass and use of agents to counteract tissue water accumulation during the ischemic and reperfusion intervals strongly influences postischemic cardiac performance. Further, these data suggest that the composition of the perfusate may have a greater influence on the functional recovery of the heart than the composition of various CPSs.
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PMID:Adequacy of the perfusate: its influence on successful myocardial protection. 713 9

The effect of different metabolic inhibitors on the induction of spontaneous rhythms by strophanthidin was studied in canine cardiac Purkinje fibers perfused in vitro. Both the electrical and mechanical activity were recorded. Strophanthidin caused its usual effects (an increase and then a decrease in force, a steepening of diastolic depolarization, spontaneous rhythms and inexcitability, but no contracture). When strophanthidin administration was repeated in the presence of depressed oxidative phosphorylation (antimycin and hypoxia), the force increased less and spontaneous rhythm occurred without the development of contracture. When strophanthidin was administered in the presence of blockade of glycolysis (iodoacetic acid and 2-deoxy-D-glucose), strophanthidin increased force even more than in the control test but steepened diastolic depolarization less or not at all and induced contracture. In some preparations, spontaneous rhythms developed but then only before the development of contracture. Hypothermia also increased the duration of the twitch and prevented the oscillatory potentials. Strophanthidin-induced arrhythmias were present in hypoxia but were prevented in hypoxia plus 2-deoxy-D-glucose. When metabolic blockade was severe (irreversible stage of antimycin action), contracture also developed, but spontaneous activity failed to appear. It is concluded that the oscillatory potentials induced by cardiac steroids are sensitive to blockade of glycolysis or severe metabolic blockade, possibly as a consequence of an impaired reuptake of calcium into sarcoplasmic reticulum.
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PMID:The effect of metabolic inhibitors on strophanthidin-induced arrhythmias and contracture in cardiac purkinje fibers. 728 19


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