Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 39-year-old man presented with multiple intracranial cavernous malformations manifesting as intractable seizures persisting for more than 20 years. He underwent gamma knife radiosurgery (GKRS) for right frontal and left temporal cavernous malformations. He began to suffer from progressive left hemiparesis and inattention 2 years 5 months after the GKRS. Magnetic resonance imaging showed abnormal ring enhancement and extensive brain edema around the right frontal lesion. Conservative therapies such as external decompression, low-dose barbiturates, and mild hypothermia had no effect on his clinical status. Stereotactic biopsy of the ring-enhanced area demonstrated gliosis. Signs of cerebral herniation appeared, so we performed partial resection of the right frontal lobe. His symptoms recovered immediately. Subsequent hyperbaric oxygen (HBO) therapy significantly improved the extensive brain edema. Delayed radiation necrosis associated with potentially fatal brain edema may occur after GKRS for cavernous malformations. Internal decompression and subsequent HBO therapy were very effective for the treatment of these lesions.
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PMID:Delayed radiation necrosis with extensive brain edema after gamma knife radiosurgery for multiple cerebral cavernous malformations--case report. 1296 6

Acute liver failure results in encephalopathy and brain edema that is characterized by astrocytic cell swelling. Molecular biological techniques have led to the identification of alterations in expression of several genes coding for key astrocytic proteins in acute liver failure. Such proteins include amino acid transporters, structural proteins, the endothelial cell glucose transporter GLUT-1, the mitochondrial "peripheral-type" benzodiazepine receptor, and the water channel protein aquaporin IV. Magnetic resonance spectroscopic studies reveal increased brain lactate concentrations that are positively correlated with severity of encephalopathy and brain edema in acute liver failure, suggesting a deficit of cellular oxidative capacity and impending brain energy failure. Mild hypothermia prevents brain edema in acute liver failure, and mechanisms responsible for this beneficial effect include reduced blood-brain ammonia transfer as well as normalization of astrocytic amino acid transport and brain energy metabolism. Further elucidation of the molecular mechanisms responsible for brain edema and encephalopathy in acute liver failure will undoubtedly lead to novel treatment strategies for these complications.
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PMID:Molecular neurobiology of acute liver failure. 1452 78

Aquaporins (AQPs) are a family of water-selective transporting proteins with homology to the major intrinsic protein (MIP) of lens, that increase plasma membrane water permeability in secretory and absorptive cells. In this study, we investigated the effect of mild hypothermia on the expression of AQP4, AQP5 and AQP9 in rat astrocytes cultured under hypoxic conditions. At 37 degrees C, a marked decrease in the expression of AQP4, AQP5 and AQP9 mRNAs was observed. However, at 32 degrees C (mild hypothermia), the expression of AQP5 mRNA was restored to its basal level. Interestingly, under mild hypothermia AQP4 mRNA expression transiently decreased and then increased about two-fold; while AQP9 mRNA expression decreased the same as at 37 degrees C. The changes in the expression of AQP4 and AQP9 proteins were confirmed by Western blot analysis. The restoration of the AQP4 and AQP5 expression at 32 degrees C from the hypoxia-induced decrease at 37 degrees C may play an important role in the reduction of brain edema under hypothermic conditions.
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PMID:Effect of mild hypothermia on the expression of aquaporin family in cultured rat astrocytes under hypoxic condition. 1463 Mar 48

The principal cause of mortality in patients with acute liver failure (ALF) is brain herniation resulting from intracranial hypertension caused by a progressive increase of brain water. In the present study, ex vivo high-resolution 1H-NMR spectroscopy was used to investigate the effects of ALF, with or without superimposed hypothermia, on brain organic osmolyte concentrations in relation to the severity of encephalopathy and brain edema in rats with ALF due to hepatic devascularization. In normothermic ALF rats, glutamine concentrations in frontal cortex increased more than fourfold at precoma stages, i.e. prior to the onset of severe encephalopathy, but showed no further increase at coma stages. In parallel with glutamine accumulation, the brain organic osmolytes myo-inositol and taurine were significantly decreased in frontal cortex to 63% and 67% of control values, respectively, at precoma stages (p<0.01), and to 58% and 67%, respectively, at coma stages of encephalopathy (p<0.01). Hypothermia, which prevented brain edema and encephalopathy in ALF rats, significantly attenuated the depletion of myo-inositol and taurine. Brain glutamine concentrations, on the other hand, did not respond to hypothermia. These findings demonstrate that experimental ALF results in selective changes in brain organic osmolytes as a function of the degree of encephalopathy which are associated with brain edema, and provides a further rationale for the continued use of hypothermia in the management of this condition.
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PMID:Selective alterations of brain osmolytes in acute liver failure: protective effect of mild hypothermia. 1474 28

Edaravone, a novel free radical scavenger, has been reported to reduce ischemic damage in rats subjected to transient focal ischemia. The aim of this study is, therefore, to investigate the effect of a combined therapy with edaravone and mild hypothermia of 35 degrees C. Sprague-Dawley rats were subjected to MCA occluding an intraluminal suture technique for 2 hrs. The rats were reperfused for 24 h and decapitated for infarct and edema analysis. Animals were randomly devided into four groups: (I) vehicle + normothermia (control) (II) vehicle + mild hypothermia (III) Edaravone + normothermia (IV) Edaravone + mild hypothermia. Mild hypothermia alone had no reduction of the brain damage. The edaravone alone significantly reduced edema volume. The combined treatment with edaravone and mild hypothermia reduced both infarct and edema volume. In addition, this treatment provided for the best functional outcome. These results demonstrate that free radical scavenger, edaravone attenuates brain edema and that the combined therapy with edaravone and mild hypothermia significantly reduces not only edema but also infarct on transient focal cerebral ischemia in rats. The neuroprotective effects seen in this study may be due to the combined interaction of antiedema activity between edaravone and mild hypothermia, suppressing free radical production.
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PMID:The neuroprotective effect of a free radical scavenger and mild hypothermia following transient focal ischemia in rats. 1475 35

Brain edema is an important clinical complication of intracerebral hematoma (ICH). Hypothermia has been employed as an effective neuroprotective treatment on cerebral ischemia and contusional brain injuries. In this study, we attempted to evaluate the effects of mild hypothermia (35 degrees C) on brain edema formation at 48 hours after ICH in the rat. Brain hypothermia started at 6, 12 and 24 hours after the induction of hematoma (HT6; n = 6, HT12; n = 11, HT24; n = 6). Brain water contents in the basal ganglia was significantly reduced in the rats treated with mild hypothermia compared with the normothermic rats (NT; 82.0 +/- 0.04% vs. HT6; 78.6 +/- 0.09%: p < 0.01, HT12; 79.7 +/- 0.05%.: p < 0.01, HT24; 79.7 +/- 0.05%: p < 0.01). Differences in the brain water content were not significant among the hypothermic subgroups. The BBB disruption to Evan's blue was significantly reduced with hypothermia compared with the normothermic rats in the ipsilateral basal ganglia (42.3 +/- 4.0 vs. 23.0 +/- 5.2 ng/g wet tissue; p < 0.05). Hypothermic treatment tended to inhibit the accumulation of polymorphonuclear (PMN) leukocytes in the lesion compared with the normothermic treatment (0.78 +/- 0.13 vs. 0.51 +/- 0.16 deltaAbs/mg tissue). This study indicates that hypothermic treatment significantly reduces the brain edema formation after ICH in rats.
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PMID:Effect of hypothermia on brain edema formation following intracerebral hemorrhage in rats. 1475 85

A 24-year-old woman was struck on the head by a hammer. Because of early signs and symptoms of intercranial hypertension, she underwent surgery for elevation of the depressed fragments which was compressing the superior sagittal sinus (SSS). After operation, the intracranial pressure (ICP) once decreased, but it gradually increased again. After hypothermia and barbiturate therapy, she recovered fully except for partial visual field defect due to brain contusion. A carotid angiogram 28 days after injury revealed complete occlusion of the whole SSS with good collateral circulation. After brain edema had subsided, a follow-up angiogram revealed normal blood flow through the SSS. Elevation of depressed bony fragments is required for a case presenting with early signs and symptoms of intracranial hypertension due to sinus compression. In a case with severe destruction of the SSS, one needs to know that re-occlusion of the dural sinus may occur after surgical recanalisation.
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PMID:Re-occlusion of the superior sagittal sinus after surgical recanalisation. 1497 31

Brain edema and consequent increase in intracranial pressure is a major complication of acute liver failure (ALF) and is a major cause of death in this condition. Rapid accumulation of ammonia in brain has been implicated in the pathogenesis of brain edema in ALF. Increased brain ammonia may cause brain swelling via the osmotic effects of an increase in astrocytic glutamine concentration or by inhibition of glutamate removal from brain extracellular space. Acute liver failure results in altered expression of several genes in the brain, some of which code for proteins involved in central nervous system function such as the glutamate transporter GLT-1, the astrocytic structural protein, glial fibrillary acidic protein, and the water channel protein, aquaporin IV. Loss of expression of GLT-1 results in increased extracellular brain glutamate. Therapeutic measures currently used to prevent and treat brain edema in acute liver failure include mannitol; strategies aimed at lowering of gut ammonia production are generally ineffective. Studies in experimental animals suggest that mild hypothermia or the use of L-ornithine-L-aspartate may be useful in the prevention of brain edema in these patients.
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PMID:Brain edema in acute liver failure. 1502 58

Opening of the blood-brain barrier (BBB) and consequent edema are known to intensify 24-72 h after ischemic stroke, and research on potential ameliorative therapies in animal models may lead to improved clinical treatments to prevent brain swelling and the secondary damage it causes. In this study, post-ischemic hypothermia treatment, which is an established neuroprotective strategy, was examined for its ability to prevent delayed BBB opening in a rat model of global ischemia. Anesthetized, normothermic SD rats (340-380 g) underwent 20 min of two-vessel (carotid) occlusion plus hypotension (2VO ischemia, between 0900-1100 h). Marked cortical BBB leakiness, which developed overnight, was indicated at sacrifice 24 h post-2VO by an average six- to eightfold increase above baseline in transfer constant values (K(i) ) for rate of blood to brain diffusion of intravenously delivered [(3)H]sucrose. A post-2VO treatment involving whole body cooling to 31.5 degrees-32.5 degrees C, maintenance for 6 h and rewarming to normothermia, significantly reduced BBB leakiness at 24 h, whether cooling was initiated immediately after reperfusion, or after a 1-h delay, but not after 2-h delay. Immediate hypothermia treatment reduced overall tissue injury at 24 h as evidenced by an assay of mitochondrial succinate dehydrogenase activity, and also reduced brain edema. By contrast, treatment of rats with the anti-inflammatory drugs cyclosporine A or minocycline offered no protection of BBB or mitochondria. It is concluded that hypothermic alteration of critical events during the first 2 h after prolonged ischemia powerfully mitigates the BBB damage and associated events that normally develop 24 h later.
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PMID:A two-hour window for hypothermic modulation of early events that impact delayed opening of the rat blood-brain barrier after ischemia. 1535 91

The development of encephalopathy in patients with acute liver injury defines the occurrence of liver failure. The encephalopathy of acute liver failure is characterized by brain edema which manifests clinically as increased intracranial pressure. Despite the best available medical therapies a significant proportion of patients with acute liver failure die due to brain herniation. The present review explores the experimental and clinical data to define the role of hypothermia as a treatment modality for increased intracranial pressure in patients with acute liver failure.
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PMID:Hypothermia in acute liver failure. 1555 17


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