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

Core body temperature is normally rigidly regulated by effective thermoregulatory responses that are triggered by small deviations in core and skin temperature. All general anesthetics so far tested markedly impair thermoregulatory control, increasing the range of temperatures not triggering protective responses by approximately 20-fold. Inhibition of thermoregulatory control--and reemergence of protective responses--are major factors influencing intraoperative temperature. Mild hypothermia provides dramatic protection against cerebral ischemia and therefore is frequently indicated during neurosurgery. Hypothermia to core temperatures near 34 degrees C can usually be instituted passively so long as thermoregulatory vasoconstriction is inhibited by sufficient anesthesia or neurosurgery per se. When core temperature must be rapidly reduced, or reduced to values approaching 32 degrees C, active cooling will usually be needed. Forced air appears to be the most effective clinically practical cooling method. Mild hypothermia is also associated with serious complications including myocardial ischemia, impaired resistance to surgical wound infections, coagulopathies, and postoperative shivering. Consequently, patients deliberately made hypothermic during neurosurgery should subsequently be actively rewarmed.
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PMID:Deliberate mild hypothermia. 788 Dec 39

Moderate hypothermia has been shown to have therapeutic utility in the treatment of cerebral ischemia and to attenuate the rise in interstitial concentrations of the excitatory amino acid neurotransmitter L-glutamate. In this study, the influence of hypothermia on traumatic brain injury (TBI) was assessed using a controlled cortical impact model. Rats were cooled to 32.0-33.0 degrees C at least 30 min before injury and maintained at this temperature for 2 h after injury. The influence of hypothermia on the immediate increase in interstitial concentrations of aspartate and glutamate and the volume of the resultant lesion 14 days after TBI was then determined. The volume of the lesion (mean +/- SEM) in hypothermic animals (8.2 +/- 1.3 mm3, n = 9) was significantly smaller than that of normothermic animals (13.2 +/- 1.7 mm3, n = 8). By contrast, TBI-induced increases in dialysate concentrations of aspartate and glutamate were similar at the two temperatures. Thus, aspartate content (nmol/10 min) in animals maintained at 37.0-37.5 degrees C (n = 6) and 32.0-33.0 degrees C (n = 6) increased from respective mean preinjury values of 0.05 +/- 0.02 and 0.08 +/- 0.02 to much larger peak values (0.78 +/- 0.13 and 0.71 +/- 0.09, respectively). Similarly, under normothermic conditions glutamate content (nmol/10 min) increased from 0.13 +/- 0.03 to 3.08 +/- 0.52 and from 0.19 +/- 0.06 to a peak value of 3.09 +/- 0.26 under hypothermic conditions. These data clearly demonstrate the cytoprotective action of moderate hypothermia and further suggest that this action is not mediated by attenuation of the rise in interstitial concentrations of aspartate and glutamate.
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PMID:Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate. 790 37

Hypothermia is of proven benefit in cerebral ischemia, and may be of benefit in blunt head injury. Peritoneal dialysis is a fast, effective method of inducing generalized hypothermia. A case is reported in which peritoneal dialysis was used to induce mild hypothermia (34.5-36 degrees C) in a patient who sustained a severe head injury, with intracranial hypertension unresponsive to hyperventilation, osmotic diuresis, and barbiturate coma. Hypothermia was associated with prompt control of temperature and intracranial pressure. Peritoneal dialysis is a useful method for inducing hypothermia in the blunt head-injured patient.
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PMID:Peritoneal dialysis to induce hypothermia in a head-injured patient: case report. 797 24

Cerebral hypothermia treatment of critical brain injury patients was studied based on the management and control of cerebral thermo-pooling, synaptic excitation, hypermetabolic demand, and the systemic critical condition of the metabolic reserve. The initial pathophysiological changes after trauma included a progressive increase in brain tissue temperature. Such cerebral thermo-pooling, which reached a maximum of 43.8 degrees C, can change or damage the vascular proteins directly. The brain tissue temperature was influenced by four factors: 1. the cerebral metabolism, 2. the systemic excess energy metabolism, 3. the CPP that carries the systemic energy to the brain tissue, and 4. the cerebral blood flow that leads to washout of brain tissue temperature. Mild cerebral hypothermia (32-33 degrees C) managed by the whole body compartment cooling technique in the critical conditions of diffuse brain injury patients (GCS < 4) produced a good recovery in 8 of 10 patients. Continuous monitoring of the jugular venous oxygen saturation and BTT/TMT was effective for evaluating cerebral ischemia and oxygen metabolic disturbances even during cerebral hypothermia treatment.
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PMID:Systemic management of cerebral edema based on a new concept in severe head injury patients. 797 43

The aim of the present study was to evaluate critically the protection afforded by hypothermia against ischemic injury to the hippocampus. Hypothermic treatment was applied selectively to the brain during a 5 min carotid artery occlusion in gerbils. Following a period of recovery, two independent measures were used to assess hippocampal function: (1) an open field test of spatial memory (assessment was made during the first 10 d after ischemia) and (2) measurement of evoked potentials from area CA1 in hippocampal slices (3 weeks after the ischemic episode). The functional outcome portrayed by these tests was compared to a morphological evaluation of CA1 pyramidal cells at three rostrocaudal levels. All evaluations were carried out in the same animals. We found converging evidence that intraischemic hypothermia provides virtually complete protection against a 5 min episode of cerebral ischemia. Animals treated with hypothermia performed as well as sham-operated controls in a spatial memory task, had field potentials that were indistinguishable from normal animals and CA1 cells appeared normal when assessed histologically. In contrast, ischemia at normothermia resulted in a deficit in open field behavior (p < 0.01), diminished field potentials in stratum radiatum (p < 0.01), and near total loss of pyramidal cells in dorsal CA1 (p < 0.01). There was a remarkably high correlation between these diverse measures (r ranged from 0.7 to 0.9, p < 0.01), which provides strong support for the use of hypothermia as an effective treatment for ischemia. This study introduces a novel approach for the evaluation of putative anti-ischemic treatments: combining behavioral, electrophysiological, and histological measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Direct measurement of brain temperature during and after intraischemic hypothermia: correlation with behavioral, physiological, and histological endpoints. 799 7

Intra-ischemic moderate hypothermia generally protects the brain against ischemic cell death, while hypothermia instigated several hours into the reperfusion phase is considered to be less effective. Here we report the effect of hypothermia (32.5 degrees - 33.5 degrees C) of 5-h duration, initiated at 2, 6, 12, 24 and 36 h into the recirculation phase following 10 min of transient cerebral ischemia, on ischemic neuronal injury in the hippocampus and striatum of the rat. Hypothermia induced at 2 h, and 6 h postischemia reduces neuronal damage in the entire hippocampal CA1 region by approximately 50%. In the lateral CA1 region hypothermia induced at 12 h postischemia, significantly mitigates necrosis. When initiated at 2 h postischemia, but not later, protection was also observed in the striatum. Hypothermia induced 24 and 36 h postischemia was ineffective. A period of hypothermia of 5 h, initiated 2 h postischemia, was required for marked neuronal protection in the CA1 region, while 3.5-h hypothermia decreased neuronal damage by approximately 10% and 30 min hypothermia was ineffective. The clinical implications of the data are that extended period of hypothermia initiated long into the recovery phase following ischemia may prove beneficial. Hypothermia protects brain regions displaying rapid as well as delayed neuronal damage, and a minimal time of hypothermia is required for effective neuronal protection. Also, strict temperature control for up to 24 h postischemia may be required for proper assessment of the efficacy of cerebro-protective drugs.
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PMID:Moderate hypothermia mitigates neuronal damage in the rat brain when initiated several hours following transient cerebral ischemia. 801 66

Experimentally, focal and global cerebral ischemia are markedly affected by small changes in brain temperature. Mild hypothermia greatly ameliorates and mild hyperthermia markedly exacerbates ischemic-induced neuronal injury. Mild hypothermia not only protects against neuronal injury but also improves clinical outcome. This effect depends on the temperature of the brain both during and after the ischemic episode. Clinical and laboratory evidence concerning the value of hypothermia and the danger of hyperthermia in acute ischemia are presented. Potential mechanisms of action of hypo- and hyperthermia in ischemic injury are also addressed. The need to treat fever in acute cerebral ischemia, even if evidence is only empiric, and the intriguing possibility of using mild hypothermia to treat acute cerebral infarction are discussed.
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PMID:Hypothermia as a potential treatment for cerebral ischemia. 811 May 95

Hypothermia provides significant protection when initiated during or after cerebral ischemia in vivo. However, the mechanisms producing this protective effect are not known. Astroglial cultures were prelabeled with [3H]arachidonic acid. Hypothermia reduced both cellular injury and release of [3H]-labeled arachidonic acid metabolites during combined glucose-oxygen deprivation. Inhibition of phospholipid degradation may be one of the mechanisms that contributes to the protective effect of hypothermia.
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PMID:Hypothermia decreases astroglial injury and arachidonate release during combined glucose-oxygen deprivation. 813 Oct 67

The effect of manipulating the brain temperature during cerebral ischemia was investigated in Wistar rats subjected to 30 min 4-vessel occlusion. Three brain temperature profiles were compared: 1. Spontaneous decrease in brain temperature during ischemia from 36 to 31 degrees C (spontaneous hypothermia; n = 5); 2. Constant brain temperature of 30 degrees C induced by selective head cooling (induced hypothermia; n = 5); and 3. Constant brain temperature of 36 degrees C induced by selective heating of the head (normothermia; n = 5). The core temperature was maintained constant at 37 degrees C in all groups. In the spontaneously hypothermic brains, 16% of the CA1 neurons survived after 30 min ischemia. Induced hypothermia significantly increased this percentage to 69%, but maintenance of the brain temperature at normothermia decreased neuronal survival to 1%. Normothermia of the brain also led to morphological injury outside the vulnerable regions, greater variability of the morphologic lesions, an increase in mortality, a marked loss of body weight, and prolongation of EEG suppression, as compared to in both hypothermic groups. These findings clearly demonstrate that maintaining the brain temperature at normothermia by selective heating of the head aggravates ischemic injury and, in consequence, should not be used to investigate the effectiveness of protective drugs for brain ischemia.
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PMID:[Temperature effect on ischemic brain injury]. 813 97

The cerebroprotective effects of mild and moderate hypothermia cannot be explained solely by a temperature-induced decrease in cerebral metabolic rate. This study examined the effects of graded hypothermia (32 degrees C, 28 degrees C, and 22 degrees C, vs 38 degrees C) on periischemic extracellular hippocampal glutamate concentrations in the New Zealand White rabbit. Global cerebral ischemia (15 min) was produced by a combination of neck tourniquet inflation and induction of systemic hypotension. Glutamate, an important mediator of ischemic neuronal injury, was measured using in vivo microdialysis and high-performance liquid chromatography. Mean extracellular glutamate concentrations increased by 11 microM in the 38 degrees C group during the ischemic period. Glutamate increased by < 1 microM in the 32 degrees C and 28 degrees C groups and by 3 microM in the 22 degrees C group. Thus, mild degrees of hypothermia profoundly reduced glutamate release during ischemia. This reduction greatly exceeded the estimated temperature-induced decrease in cerebral metabolic rate. We conclude that hypothermic inhibition of glutamate release during episodes of transient ischemia may significantly contribute to neuronal protection.
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PMID:Effects of hypothermic metabolic suppression on hippocampal glutamate concentrations after transient global cerebral ischemia. 816 Sep 88


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