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

1 The prolongation of pentobarbitone sleeping by five benzodiazepines, administered by prior intraperitoneal injection, was measured in mice. The pentobarbitone was injected either intraperitoneally or intracerebroventricularly. For each benzodiazepine, the prolongation was dose-related and differences in potency between benzodiazepines were not marked. 2 The percentage prolongation of sleeping times produced by most of the benzodiazepines was greater when the pentobarbitone was given intracerebroventricularly and was explained by a preferential addition of CNS depressant effects associated with this route. 3 To test whether the action of intraperitoneally administered pentobarbitone had been influenced by a metabolic component, the effects of nitrazepam on drug metabolism, measured by changes in plasma phenazone levels in the mouse, were studied. Nitrazepam (32 mg/kg, i.p.) produced a 23% reduction in the rate of phenazone metabolism. 4 Nitrazepam was also shown to have produced a transient fall in body temperature. Calculations based on Q10 values suggested that this hypothermia accounted, at most, for half the metabolic change measured.
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PMID:Some observations on the mechanism of benzodiazepine-barbiturate interactions in the mouse. 1 17

1. The response of left atrial type B receptors to hypothermia and its effect on the V-wave pressure-receptor activity relationship was studied in ten anaesthetized and thoracotomized dogs. Hypothermia was produced by surface cooling of the animal. 2. With the drop in the body temperature there was a corresponding fall in the peak frequency of discharge. Reduction in the number of impulses per cardiac cycle and the average resting activity of these receptors became significant only when body temperature fell below 31 degrees C. The Q10 for these receptors is about 2.5, i.e., similar to that for the other mechanoreceptors and consistent with the view that these receptors are in parellel with the muscle fibres. 3. The V-wave pressure-receptor activity relationships were not altered by acute hypothermia.
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PMID:Left atrial type B receptor response during hypothermia in dogs. 51 8

During daily torpor and hibernation metabolic rate is reduced to a fraction of the euthermic metabolic rate. This reduction is commonly explained by temperature effects on biochemical reactions, as described by Q10 effects or Arrhenius plots. This study shows that the degree of metabolic suppression during hypothermia can alternatively be explained by active downregulation of metabolic rate and thermoregulatory control of heat production. Heat regulation is fully adequate to predict changes in metabolic rate, and Q10 effects are not required to explain the reduction of energy requirements during hibernation and torpor.
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PMID:Body temperature and metabolic rate during natural hypothermia in endotherms. 149 28

In pigeons, during shallow nocturnal hypothermia induced by food deprivation, body temperature falls to values between 35 degrees C and 38 degrees C. Body temperature, oxygen consumption, and arterial blood pH and PCO2 were recorded during the entrance into such nocturnal hypothermic periods. In vivo pH was kept constant, while in vivo PCO2 increased slightly during hypothermia. This caused the temperature-corrected value of pH (pH*, measured at 40 degrees C) to fall by -0.014 units/degrees C, and the total CO2-content to rise by 3.2 mM, an increase of 16%. These changes in the acid-base balance represent, in effect, a respiratory acidosis that closely parallels the normal buffer line for pigeons. Q10 values, relating oxygen uptake to body temperature, were higher than 4.0 at the very beginning of the entrance into hypothermia, indicating that the metabolic rate was actively inhibited. However, the present results do not indicate any relationship between the acidosis and the inhibition of the metabolic rate.
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PMID:Oxygen consumption and acid-base balance during shallow hypothermia in the pigeon. 162 38

Temperature has pronounced and complex effects on cellular physiology. Rates of enzymatic processes display an exponential change with temperature, as expressed by the Q10 relationship. The basis of these effects may be temperature induced phase transitions in membrane lipids and protein associated water, effects on bulk water and effects on the relationship between water and inorganic solutes. Hypothermia may be lead to a collapse in ionic regulation, leading to an uncontrollable and lethal calcium influx. Subfreezing temperatures may cause injury due to cellular freezing with subsequent excessive osmotic swelling, lyotropic effects or excessive osmotic shrinking due to extracellular freezing. Cells may protect themselves by freeze avoidance accomplished by removal of ice nucleators, production of proteinaceous antifreeze agents and accumulation of polyols. Alternatively they may secure extracellular freezing by production of extracellular ice nucleating agents, and counteract lyotropic effects and osmotic shrinking by accumulation of polyols which reduce ice content in a colligative manner.
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PMID:Hypothermia and cellular physiology. 181 67

We tested the hypotheses that hypoxic toads (Bufo marinus) in a thermal gradient would select a lower than normal temperature and that this behavioral response would be beneficial. Under normoxic conditions, selected body temperature was 24.2 +/- 3.6 degrees C. When inspired O2 was 10% or less, mean selected temperature decreased to 15.3 +/- 2.4 degrees C. The theoretical advantages of hypoxia-induced hypothermia we tested include (1) a reduction of oxygen uptake (VO2) by a Q10 effect; (2) increased arterial saturation (SaO2), (3) a decreased ventilatory response, and (4) a decreased stress response. Gas exchange, hematocrit, hemoglobin, SaO2, PaO2 and pH were measured at 25 degrees C (normal preferred temperature) and 15 degrees C (hypoxia preferred temperature) in toads breathing normoxic or hypoxic gas mixtures. During graded hypoxia at 15 degrees C, SaO2 was significantly increased and VO2 was significantly reduced compared with 25 degrees C. Graded hypoxia did not significantly affect VO2 at 25 degrees C, despite evidence for increased ventilation at that temperature (increased pH and respiratory exchange ratio, RE). At 15 degrees C, graded hypoxia had a significant effect on VO2 only at an inspired O2 of 4%. Increased RE with hypoxia was significant at 25 degrees C but not at 15 degrees C. Hematocrit and [hemoglobin] rose significantly during graded hypoxia at 25 degrees C but did not change at 15 degrees C. Toads exposed to 10% O2 (the value that elicits behavioral hypothermia) showed a significant respiratory alkalosis at 25 degrees C but not at 15 degrees C. Likewise, hypoxia caused a significant drop in SaO2 and PO2 at 25 degrees C. Cooling to 15 degrees C during hypoxia caused a significant rise in SaO2 but no change in PaO2. In conclusion, behavioral hypothermia is a beneficial response to hypoxia in Bufo marinus.
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PMID:Physiological significance of behavioral hypothermia in hypoxic toads (Bufo marinus). 194 Jul 67

Cerebral protection by hypothermia is commonly attributed to cerebral metabolic suppression. However, at temperatures below 28 degrees C, the relationship of temperature to cerebral metabolic rate of oxygen consumption (CMRO2) has not been well characterized. Accordingly, the relationship between brain temperature and CMRO2 was determined in eight dogs during cooling from 37 to 14 degrees C while the EEG was continuously monitored. Cardiopulmonary bypass was initiated and control measurements were made at 37 degrees C during anesthesia with nitrous oxide 50-60% inspired and morphine sulfate 2 mg.kg-1 intravenously (iv). Upon cooling to 27 degrees C, the nitrous oxide was discontinued and the morphine was antagonized with naloxone 2 mg iv. Measurements were repeated at 27, 22, 18, and 14 degrees C and in four dogs again at 37 degrees C after nitrous oxide 50-60% had been reestablished at 27 degrees C along with administration of morphine sulfate 2 mg.kg-1. For each temperature interval, the temperature coefficient (Q10) for CMRO2 was calculated (Q10 = CMRO2 at x degrees C divided by CMRO2 at [x - 10] degrees C). Between 37 and 27 degrees C the Q10 was 2.23, but between 27 and 14 degrees C the mean Q10 was doubled to 4.53. With rewarming to 37 degrees C, CBF and CMRO2 returned to control levels, and brain biopsies revealed a normal brain energy state. During cooling, the EEG developed burst suppression at or below 22 degrees C. With further cooling, the periods of suppression increased; however, burst activity continued in seven of eight dogs even at 14 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship among canine brain temperature, metabolism, and function during hypothermia. 206 37

The direct effect of hypothermia on the inhibition of insulin secretion may result from inhibition of the availability of energetic substrates and/or the lack of metabolic signals. In order to verify this hypothesis, the insulin secretion and the main metabolic glucose pathways were measured during the incubation of rat islets. In the presence of 16.7 mmol glucose/l and at 37 degrees C, insulin secretion was 925 +/- 119 microU/2 h per ten islets. With the same experimental conditions, glucose utilization, determined as the formation of 3H2O from [5-3H]glucose was 2225 +/- 184 pmol/2 h per ten islets, glucose oxidation measured as the formation of 14CO2 from [U-14C]glucose was 673 +/- 51 pmol/2 h per ten islets, pentose cycle determined as the formation of 14CO2 from either [1-14C]glucose or [6-14C]glucose was 37 +/- 5 pmol/2 h per ten islets; glucose oxidation by the tricarboxilic acid cycle, calculated to be the difference between glucose oxidation and pentose cycle values, was 636 pmol/2 h per ten islets. Hypothermia highly inhibited glucose-induced insulin secretion and glucose utilization. Inhibition of insulin secretion was partial at 27 degrees C since it was 2.5 times lower than that at 37 degrees C, and it was complete at 17 degrees C. Glucose oxidation in the tricarboxilic acid cycle was markedly inhibited by hypothermia since the inhibition coefficient (Q10) between 37 and 27 degrees C was 5. In contrast, glucose oxidation in the pentose phosphate shunt was enhanced at 27 degrees C, reaching 92 +/- 17 pmol/2 h per ten islets, and it was inhibited relatively little at 17 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of low temperatures on glucose-induced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat. 218 49

The management of blood pH during hypothermia remains controversial. The present study was designed to determine whether hemodynamics and oxygen consumption during hypothermia are different between the alpha-stat and pH-stat strategies. Theoretical considerations of enzyme kinetics suggest that the alpha-stat strategy would result in a higher oxygen consumption during hypothermia. Because hypothermia is used to decrease oxygen consumption for protection during ischemia, a pH scheme that results in a greater oxygen demand for any level of ischemia would be detrimental. The core temperature of 22 dogs was lowered to 26 degrees C by combined surface cooling and gastric irrigation. Either the alpha-stat (N = 9) or the pH-stat (N = 13) pH strategy was used. The arterial pressure was different between the two groups at 26 degrees C (65 +/- 6 vs 85 +/- 6 mm Hg, alpha-stat vs pH-stat, respectively, P less than 0.05). Neither systemic oxygen consumption nor the Q10 was different between groups. There were no differences in any other hemodynamic parameters. In summary, during moderate hypothermia alpha-stat pH management results in an arterial pressure lower than that of pH-stat management, possibly resulting in improved peripheral perfusion. Despite theoretical predictions, the alpha-stat pH scheme does not result in an oxygen consumption higher than that of the pH-stat scheme.
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PMID:Hemodynamics and metabolism during surface-induced hypothermia in the dog: a comparison of pH management strategies. 231 95

Chronic pontile cats (without hypothalamo-hypophysis) were kept during 4 days at central T (TC) between 37.5 and 30.8 degrees C at stable ambiant T (TA) between 28.5 and 23 degrees C. The vasomotor index of the forepaw was chosen for studying change in vasomotricity. Small and slow variations of TA (+1.5 degrees C) around 27 degrees C were followed by thermoregulatory response since a progressive decrease of TA under 27 degrees C led to vasoconstriction and increase of TC while progressive increase of TA above 27 degrees C led to vasodilatation and decrease of TC. However rapid and large decrease of TA under 27 degrees C (24-23 degrees C) led to the expected hypothermia with decrease of TC but without vasoconstriction. Paradoxical sleep (PS) amounts were strongly correlated with TC. At TC above 35.5 degrees C PS was almost totally suppressed while it increased significantly under 35 degrees C (Q10 = 0.10). Under 35 degrees C at stable TC and TA, PS occurred with an endogenous circahoral rhythm which did not vary significantly between 35 and 32 degrees C. These results strongly suggest that in pontile cats, PS is both gated and regulated by TC, while TC is regulated by pontobulbar vasomotor systems in response to TA. The putative role of the ventro-lateral medulla, in controlling both vasomotricity, TC and the excitability of the locus coeruleus is discussed in relation with PS.
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PMID:[Hypothermia and paradoxical sleep. I. Pontile cats without hypothalamo-hypophysis]. 314 39


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