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

Most animals respond to a shortage of oxygen by lowering their body temperature. This response, mediated by behavior and physiological means, reduces oxygen demand via the Q10 effect, and should therefore be adaptive. This article reviews the occurrence of this response within the animal kingdom, the possible mechanisms and mediators of the response, and the physiological significance of hypoxia-induced hypothermia.
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PMID:Oxygen as a modulator of body temperature. 872 55

Previously the authors showed that hypothermia exerts a greater effect on the cerebral metabolic rate for oxygen (CMRO2) that is associated with the maintenance of cellular viability, or "basal" CMRO2, than on electroencephalogram (EEG)-associated CMRO2 or "functional" CMRO2. On the basis of their findings, the authors hypothesized that the ratio of CMRO2 over a 10 degrees C temperature range (Q10) for basal CMRO2 was greater than that for functional and total CMRO2. They tested their hypothesis by determining the Q10 for basal CMRO2 from 38 degrees C to 28 degrees C. They measured whole-brain cerebral blood flow (CBF) and CMRO2 in six rats during progressive hypothermia at a brain temperature of 38 degrees C and, after induction of an isoelectric EEG signal (50 microV/cm) with thiopental sodium, they repeated the measurements at 38 degrees C, 34 degrees C, 30 degrees C, and 28 degrees C. In a control group (five rats), six sequential measurements of CBF and CMRO2 were made while the animals were anesthetized by 0.5% isoflurane/70% N2O/30% O2 at a brain temperature of 38 degrees C over a time span equivalent to the hypothermic group, that is, approximately 3 hours. The Q10 for basal CMRO2 calculated over 38 degrees C to 28 degrees C was 5.2 +/- 0.92. However, the decrease in basal CMRO2 between 38 degrees C and 28 degrees C was nonlinear on a log plot, revealing a two-component response: a high temperature sensitivity component between 38 degrees C and 30 degrees C with a Q10 of 12.1, and a lower temperature sensitivity component between 30 degrees C and 28 degrees C with a Q10 of 2.8. The combined overall Q10 for basal CMRO2 between 38 degrees and 28 degrees C was 5.2. The energy-requiring processes associated with these high and low temperature sensitivity components of basal CMRO2 have yet to be identified.
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PMID:The Q10 ratio for basal cerebral metabolic rate for oxygen in rats. 875 36

Since there are complex regulations of paradoxical sleep at the supra-pontine level, the chronic pontine preparation appears to be the best model for studying the mechanisms of the ultradian rhythm of PS (tau'). In these preparations, which are ectothermic, tau' is considerably dependent upon temperature conditions. a) PS never occurs above a central temperature (Tc) of 36 degrees C which constitutes the absolute threshold for PS. b) If Tc is regulated at a plateau between 34.5 degrees C and 35.5 degrees C, the duration of tau' corresponds to about 60 min (circhoral) whereas the duration of PS is 5 min, thus the cyclic ratio: tau'/duration of PS is 12. During deep hypothermia (from 35 degrees C to 25 degrees C), tau' of PS is temperature-compensated. It remains close to 60 min, so that its Q10 is about 1. c) However, in the same conditions, the duration of PS episodes increases from 5 min to 55 min, so that the Q10 of PS is 0.1 (8% at 35 degrees C - 80% at 25 degrees C). These data are discussed in the light of the present theories explaining tau' (i.e., the reciprocal inhibition between monoaminergic permissive systems and cholinergic executive systems). An increase in PS during hypothermia might be possible provided that it should be proved that permissive mechanisms are excited by heat while executive mechanisms would be cold-sensitive. But there are no data on this point. However, even this "differential thermosensitivity hypothesis" would not explain the striking fixity of tau' between 35 degrees C and 25 degrees C. For this reason, one should hypothetize that there is a temperature-compensated oscillator or pacemaker which would act upon both executive and permissive mechanisms. This oscillator would also be controlled by metabolic factors as shown by the effect of O2 and prolactin.
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PMID:[Is there a bulbar pacemaker responsible for the ultradian rhythm of paradoxical sleep?]. 891 91

A basic tenet of biology is that body temperature (Tb) has a marked effect on oxygen uptake of resting animals. For most animals, the temperature coefficient (Q10) is >> 2.5; e.g., resting oxygen uptake changes about 11% per degree C change in Tb. An important consequence of this dependence is that hyperthermia could be deleterious for hypoxic animals, particularly for oxygen sensitive organs, e.g., heart and brain. Conversely, a moderate degree of hypothermia could be beneficial during hypoxia. This concept is not new. Forced hypothermia is sometimes used in surgical procedures, particularly for heart and brain surgery. However, in many situations where hypothermia might have benefits, e.g., pediatric intensive care, it is not permitted. This is due in part to dogma and in part to the real and potential disadvantages of hypothermia, even in severely hypoxic animals. Among these in ventricular fibrillation. This is apparently preventable if blood pH is allowed to rise following the "Buffalo Curve." Another important disadvantage, were it to occur, is elevation of oxygen demand due to a thermogenic responses. However, at least in some species, the thermogenic response is blunted during hypoxia; e.g., in young rats. Furthermore, even if a thermogenic response occurs, this takes place primarily in muscles (shivering) and brown fat (non-shivering) and not in the O2-sensitive organs, heart and brain. A third disadvantage, for prolonged hypothermia, might be impairment of the immune response, a serious problem if hypoxia is combined with infection. This paper will review four aspects of behavioral fever and hypothermia: the occurrence among animals, the mechanisms and mediators that might trigger behavioral responses, and the functional significance.
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PMID:Hypothermia in hypoxic animals: mechanisms, mediators, and functional significance. 893 41

Moderate hypothermia significantly diminishes consequences of spinal and cerebral anoxia. One component of this neuroprotection has been hypothesized to be suppression of excitotoxic transmitter release. Whether this suppression is attributable to reduced hypoxic injury that induces release or an alteration of the release process itself is unclear. We sought to characterize the temperature sensitivity (Q10) of basal and evoked calcitonin gene-related peptide (CGRP) and amino acid release from dorsal horn slices of rat spinal cord over a range of temperatures from 40 to 8 degrees C. At 40 degrees C, potassium (60 mM) and capsaicin (10 microM) evoked a 21- and 32-fold increase in basal CGRP concentrations, respectively. Capsaicin had no effect on glutamate release, but potassium evoked a 2.7-fold increase. Release evoked by either potassium or capsaicin was reduced in a biphasic fashion with declining temperature. Over the range of 40 to 34 degrees C, the Q10 values for evoked release for CGRP were 11.3 (potassium) and 39.7 (capsaicin) and for glutamate, 5. 5 (potassium). Over the range of 34 to 8 degrees C, Q10 values were near unity for all evoked release (0.8 and 1.3 for CGRP and 1.2 for glutamate). Although serine, glycine, glutamine, taurine, and citrulline showed no evoked release, basal levels were reduced at temperatures below 34 degrees C. The pronounced temperature dependency of evoked transmitter release between 40 and 34 degrees C is consistent with the profound cerebral protection observed with mild hypothermia in which metabolic activity is only slightly depressed.
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PMID:Temperature dependency of basal and evoked release of amino acids and calcitonin gene-related peptide from rat dorsal spinal cord. 915 57

Hypothermia protects the brain and other vital organs during periods of ischaemia. We differentiate between mild (36-34 degrees C), moderate (33-29 degrees C), deep (28-17 degrees C) and profund (16-4 degrees C) hypothermia. During hypothermia, cerebral metabolic rate and cerebral blood flow decrease dependent on temperature. The relation between temperature and cerebral metabolism is expressed by the temperature coeffizient Q10, which is the ratio between two metabolic rates separated by 10 degrees C. The following factors contribute to decreases in cerebral blood flow seen during hypothermia: cerebral metabolic depression, decreases in cardiac output, and decreases in arterial blood pressure with pH-stat management, increases in hematocrit and in blood viscosity. Mild or moderate hypothermia reduces histopathological damage and neurological deficits if started before and during cerebral ischaemia. Hypothermia may also improve neurologic outcome if initiated following focal cerebral ischaemia, but is less effective after global ischaemic insults. Mild hypothermia appears to be safer and more effective compared to moderate hypothermia. In most instances, deep hypothermia renders neurologic outcome worse, which is most likely related to the generation of toxic metabolites and inadequate myocardial function during rewarming. The neuroprotective effects of hypothermia are related to several mechanisms along the ischaemic cascade: prevention of postischaemic hypoperfusion, reduction of functional and basal metabolism, decreased accumulation of lactic acid and oedema formation, inhibition of excitatory neurotransmitter release, prevention of Ca(++)- and Na(+)-influx, inhibition of lipid peroxidase activity, and free radical formation, stimulation of regenerative immediate early genes. The side effects of hypothermia include myocardial ischaemia, cardiac arrhythmias, decreased left ventricular contractility, coagulation abnormalities, and suppression of metabolic and immunological processes.
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PMID:[Mild and moderate hypothermia as a new therapy concept in treatment of cerebral ischemia and craniocerebral trauma. Pathophysiologic principles]. 928 20

In order to examine the effects of hypothermia on the changes in membrane potential induced by experimental ischemia (deprivation of oxygen and glucose), intracellular recordings were made from single CA1 pyramidal neurons in slice preparations of rat hippocampus. Application of ischemic medium caused irreversible changes in membrane potential consisting of an initial hyperpolarization, then a slow depolarization and a rapid depolarization. At temperatures of 35 degrees C and 37 degrees C, once the rapid depolarization occurred, readministration of oxygen and glucose failed to restore the membrane potential, a state referred to as irreversible membrane dysfunction. When the temperature was lowered to between 27 degrees C and 33 degrees C, the membrane potential returned to the control resting membrane potential in 75% of the neurons. The temperature coefficients (Q10) of the latency, the amplitude, and the maximal slope of the rapid depolarization were 2.5, 1.4 and 2.9, respectively. It is concluded that the critical neuroprotective temperature in ischemia-induced membrane dysfunction is found to be 33 degrees C in single CA1 neurons in vitro.
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PMID:Mild hypothermia protects rat hippocampal CA1 neurons from irreversible membrane dysfunction induced by experimental ischemia. 957 74

At the low temperatures of the overwintering environment of the frog Rana temporaria, small changes in ambient temperature have large effects on metabolism and behaviour, especially since Q10 values are often greatly elevated in the cold. How the overwintering aquatic frog copes with variable thermal environments in terms of its overall activity metabolism and recovery from pursuit by predators is poorly understood, as is the role of behavioural thermoregulation in furthering recovery from intense activity. Exhaustive exercise was chosen as the method of evaluating activity capacity (defined by time to exhaustion, total distance swum and number of leg contractions before exhaustion) and was determined at 1.5 and 7 degreesC. Other cohorts of frogs were examined at both temperatures to determine the metabolic (acid-base, lactate, glucose, ATP and creatine phosphate) and respiratory responses to exercise in cold-submerged frogs. Finally, temperature preference before and after exercise was determined in a thermal gradient to define the importance of behavioural thermoregulation on the recovery rates of relevant metabolic and respiratory processes. Activity capacity was significantly reduced in frogs exercised at 1.5 versus 7 degreesC, although similar levels of tissue acid-base metabolites and lactate were reached. Blood pH, plasma PCO2 and lactate levels recovered more rapidly at 1.5 degreesC than at 7 degreesC; however, intracellular pH and the recovery of tissue metabolite levels were independent of temperature. Resting aerobic metabolic rates were strongly affected by temperature (Q10=3.82); however, rates determined immediately after exercise showed a reduced temperature sensitivity (Q10=1.67) and, therefore, a reduced factorial aerobic scope. Excess oxygen consumption recovered to resting values after 5-6.25 h, and 67 % recovery times tended to be slightly faster at the lower temperatures. Exercise in the cold, therefore, provided an immediately higher factorial scope, which could be involved in the faster rate of recovery of blood lactate levels in the colder frogs. In addition, exercise significantly lowered the preferred temperature of the frogs from 6.7 to 3.6 degreesC for nearly 7 h, after which they returned to their normal, unstressed preferred temperatures. Thus, a transient behavioural hypothermia in the skin-breathing, overwintering frog may be an important strategy for minimising post-exercise stress and maintaining aerobic metabolism during recovery from intense activity.
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PMID:Does behavioural hypothermia promote post-exercise recovery in cold-submerged frogs? 992 62

This paper reviews literature on the topic of cold stress, near-drowning and hypothermia, written mainly since the last review of this type in this journal. The main effects of cold stress, especially in cold water immersion, include the "cold shock" response, local cooling causing decrements in physical and mental performance, and ultimately core cooling as hypothermia occurs. The section on cold-water submersion (near-drowning) includes discussion regarding the various mechanisms for brain and body cooling during submersion. The mechanisms for cold-induced protection of the anoxic brain are discussed with attention given to decreased brain temperature and the Q10 principle, the mammalian dive reflex and a newly considered mechanism; cold-induced changes in neurotransmitter release (i.e., glutamate and dopamine). The section on the post-cooling period includes the post-rescue collapse and subsequent rewarming strategies used in the field, during emergency transport or in medical facilities. Recent research on topics such as inhalation warming, body-to-body warming, radio wave therapy, warm water immersion, exercise, body cavity lavage, and cardiopulmonary bypass is reviewed. Information on new methods of warming, including arteriovenous anastomoses (AVA) warming (by application of heat- with or without negative pressure application-to distal extremities in an effort to increase AVA blood flow), forced-air warming, and peripheral vascular extracorporeal warming, are discussed.
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PMID:Cold stress, near drowning and accidental hypothermia: a review. 1090 37

Studies documenting the cerebral hemodynamic consequences of selective brain hypothermia (SBH) have yielded conflicting data. Therefore, the authors have studied the effect of SBH on the relation of cerebral blood flow (CBF) and CMRO2 in the forebrain of pigs. Selective brain hypothermia was induced in seven juvenile pigs by bicarotid perfusion of the head with extracorporally cooled blood. Cooling and stepwise rewarming of the brain to a Tbrain of 38 degrees C, 25 degrees C, 30 degrees C, and 38 degrees C at normothermic Ttrunk (38 degrees C) decreased CBF from 71 + 12 mL 100 g(-1) min(-1) at normothermia to 26+/-3 mL 100 g(-1) min(-1) and 40+/-12 mL 100 g(-1) min(-1) at a Tbrain of 25 degrees C and 30 degrees C, respectively. The decrease of CMRO2 during cooling of the brain to a Tbrain of 25 degrees C resulted in a mean Q10 of 2.8. The ratio between CBF and CMRO2 was increased at a Tbrain of 25 degrees C indicating a change in coupling of flow and metabolism. Despite this change, regional perfusion remained coupled to regional temperatures during deep cerebral hypothermia. The data demonstrate that SBH decreases CBF and oxygen metabolism to a degree comparable with the cerebrovascular and metabolic effects of systemic hypothermia. The authors conclude that, irrespective of a change in coupling of blood flow and metabolism during deep cerebral hypothermia, cerebral metabolism is a main determinant of CBF during SBH.
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PMID:Coupling of cerebral blood flow and oxygen metabolism in infant pigs during selective brain hypothermia. 1095 Mar 82


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