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

Acute subdural hematoma (SDH) is the most common mass lesion in severe head injury, and brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage following SDH. Hypothermia has been employed as an effective neuroprotective procedure in clinical and laboratory studies on cerebral ischemic and contusional injuries. In the present study, we used a rat acute SDH model to assess the effect of hypothermia on the intracranial pressure (ICP) and also on the brain edema formation at 4 h after hematoma induction. Mild (34 degrees C) and moderate (32 degrees C) hypothermia did not significantly affect the ICP or cerebral perfusion pressure, but they were associated with a significant lower cortical brain edema formation beneath the hematoma (81.09 +/- 0.49%, p<0.05; and 80.88 +/- 0.17%, p<0.01) when compared with the normothermic control group (81.65 +/- 0.52%). This reduction in brain edema formation was comparable to the results of MK-801 treatment (80.95 +/- 0.35%, p<0.01). The present findings indicate that hypothermia represents a potent neuroprotective strategy. The possible protective mechanisms of hypothermic protection afforded in this rat acute SDH model are discussed.
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PMID:Effects of hypothermia on intracranial pressure and brain edema formation: studies in a rat acute subdural hematoma model. 1075 25

We treated two children with influenza-associated acute encephalopathy by a combination of mild hypothermia and steroid pulse therapy. Case 1, a 2-year-and-3-month-old boy, admitted to our hospital 7 days after the onset of central nervous symptoms. The brain MRI-CT revealed laminar cortical necrosis and severe brain edema. EEG showed very low voltage. Brain edema improved by the combination therapy. He had sequelae, but was able to eat. Case 2, a 1-year-and-10-month-old boy, admitted to our hospital 5 days after the onset of central nervous symptoms. Brain MRI showed frontal dominant cortical edema. EEG showed high voltage delta bursts. The combination therapy was effective, but he remained mental handicapped. The outcome was better compared to our previous cases of acute encephalopathy. The combination therapy is intended to counteract cytokines, and was considered to be an effective treatment against acute encephalopathy associated with an influenza virus infection.
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PMID:[Effects of mild hypothermia and steroid pulse combination therapy on acute encephalopathy associated with influenza virus infection: report of two cases]. 1091 71

Brain injury due to bacterial meningitis results in a high mortality rate and significant neurologic sequelae in survivors. The objective of this study was to determine if the application of moderate hypothermia shortly after the administration of antibiotics would attenuate the inflammatory response and increase in intracranial pressure that occurs in meningitis. For this study we used a rabbit model of severe Group B streptococcal meningitis. The first component of this study evaluated the effects of hypothermia on blood-brain barrier function and markers of inflammation in meningitic animals. The second part of the study evaluated the effects of hypothermia on intracranial pressure, cerebral perfusion pressure and brain edema. This study demonstrates that the use of hypothermia preserves CSF/serum glucose ratio, decreases CSF protein and nitric oxide and attenuates myeloperoxidase activity in brain tissue. In the second part of this study we show a decrease in intracranial pressure, an improvement in cerebral perfusion pressure and a decrease in cerebral edema in hypothermic meningitic animals. We conclude that in the treatment of severe bacterial meningitis, the application of moderate hypothermia initiated shortly after antibiotic therapy improves short-term physiologic measures associated with brain injury.
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PMID:Hypothermia as an adjunctive treatment for severe bacterial meningitis. 1103 98

Despite the intensive care management of patients with large cerebral infarcts, mortality rates remain high. Conservative medical management is largely ineffective in this population. Patients at high risk for the development of massive brain edema can be identified within the first few hours of onset. This is important to remember because therapeutic benefit may require early intervention, before the brain is displaced by edema. Induced moderate hypothermia (328C to 338C) and hemicraniectomy with durotomy or duroplasty are two promising therapeutic strategies that may reduce mortality rates and improve outcomes if they are performed before irreversible brain stem injury occurs.
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PMID:Mass Effect with Cerebral Infarction. 1109 9

Recent studies have shown that thrombin plays an important role in brain edema formation after intracerebral hemorrhage (ICH). The possible mechanisms of thrombin-induced brain edema formation include blood-brain barrier (BBB) disruption and inflammatory response involving polymorphonuclear (PMN) leukocyte. Animal experiments have revealed that moderate therapeutic hypothermia improves pathological and functional outcome in various models of brain injury. In this study, we examined the effect of hypothermia on thrombin-induced brain edema formation. Effects of hypothermia on BBB permeability and the accumulation of PMN leukocytes were also determined to clarify the protective mechanism of hypothermia in this model. Anesthetized adult rats received an injection of 10 Units of thrombin into the basal ganglia. Animals were separated into the normothermic and hypothermic groups, which were housed in a room maintained at 25 degrees C and in a cold room maintained at 5 degrees C, respectively, for 24 h after the thrombin injection. The brain temperature in rats housed in a cold room reduced temporarily to approximately 30 degrees C and then gradually recovered to 35 degrees C by the end of the observation. Brain water content in the basal ganglia was significantly reduced in rats treated with hypothermia compared to the normothermic rats (84.3+/-0.2 vs. 82.4+/-0.1%; P<0.01). The decrease of brain water content was accompanied with a significant reduction in BBB permeability to Evan's blue dye and in accumulation of PMN leukocytes. This study indicates that hypothermic treatment significantly reduces thrombin-induced brain edema formation in the rat. Inhibition of thrombin-induced BBB breakdown and inflammatory response by hypothermia appear to contribute to brain protection in this model. Hypothermic treatment may provide an approach to potentially reduce ongoing edema after ICH.
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PMID:Effects of hypothermia on thrombin-induced brain edema formation. 1125 59

Mild hypothermia prevents the development of brain edema in rats with acute liver failure resulting from hepatic devascularization. Mechanistic studies performed in this model suggest that the protective effect of hypothermia results from the inhibition of blood-brain transfer of ammonia, an action which could result (at least in part) from an effect on cerebral blood flow. Hypothermia-induced reductions of brain ammonia are associated with normalization of extracellular brain glutamate concentrations in rats with acute liver failure. Studies in humans suggest that mild hypothermia is beneficial in the management of severely raised intracranial pressure, both before and after liver transplantation in patients with acute liver failure due to acetaminophen overdose. Mild hypothermia offers a potentially useful bridge therapy in patients with acute liver failure who are awaiting liver transplantation.
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PMID:Mild hypothermia prevents cerebral edema in acute liver failure. 1129 86

Brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage after subdural hematoma (SDH). Hypothermia has been used as the effective neuroprotective treatment in clinical and laboratory studies of ischemic brain injury. In this study, we have examined the rat acute SDH model to assess the effect of hypothermia upon intracranial hemodynamics and also upon ischemic brain injury 4 hours after the induction of hematoma. Moderate hypothermia (32 degrees C) did not affect the intracranial pressure nor cerebral perfusion pressure, and it significantly reduced cortical brain edema formation underneath the hematoma (80.88 +/- 0.17%; p < 0.01) compared with the normothermic control group (81.65 +/- 0.52%). This reduction in brain edema formation was comparable to the result of MK-801 (2 mg/kg) treatment (80.95 +/- 0.35%; p < 0.01). Ischemic brain damage detected by H-E staining was also significantly reduced in the hypothermia and MK-801 treated groups (59.1 +/- 12.3 mm3 and 66.4 +/- 13.8 mm3; p < 0.01 and p < 0.05) compared with the normothermic control group (86.6 +/- 20.7 mm3). In conclusion, the present study demonstrates that hypothermia is a potent neuroprotective method and an inhibition of the glutamate excitotoxic process may contribute the protective mechanisms of hypothermia in this rat acute SDH model.
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PMID:Effects of hypothermia on intracranial hemodynamics and ischemic brain damage-studies in the rat acute subdural hematoma model. 1145 84

In view of the increasing significance of mild hypothermia (32 degrees C) as an efficient procedure of neuroprotection, the present study was performed to examine the influence of this level of hypothermia on the volume of glial cells under physiological as well as under pathological conditions. The influence of mild (32 degrees C) and moderate (27 degrees C) hypothermia on cell volume and cell viability of C6 glioma cells was studied for 60 minutes in vitro. Cells were suspended in an incubation chamber under continuous control of temperature, pH and pO2. Cell volume was measured by an advanced Coulter system. Hypothermia itself was causing significant cell swelling in a dose-dependent manner, which could be prevented by omission of Na(+)-ions from the suspension medium, while the replacement of Cl(-)-ions failed to prevent cell swelling from hypothermia. Inhibition of the Na+/H(+)-antiporter with EIPA (5N-ethyl-n-isopropyl-amiloride, 50 microM) was significantly reducing the hypothermia induced cell swelling, indicating activation of the Na+/H(+)-antiporter. Conversely, mild or moderate hypothermia failed to prevent cell swelling from lactic acid, arachidonic acid or glutamate, i.e. agents which are mediating the development of cytotoxic brain edema in vivo in cerebral trauma, ischemia and other acute insults. The findings indicate that cerebral protection by hypothermia in vivo is most likely not attributable to an inhibition of cytotoxic brain edema. Further investigations, however, are required in vivo and in vitro to elucidate the hypothermia-induced swelling of glial cells in more detail, e.g. as to the role of the Na+/H(+)-antiporter.
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PMID:Influence of hypothermia on cell volume and cytotoxic swelling of glial cells in vitro. 1145 89

Patients with fulminant hepatic failure (FHF) die with brain edema, exhibiting an increased cerebral blood flow (CBF) at the time of cerebral swelling. Mild hypothermia prevents brain edema in experimental models and in humans with FHF, an effect associated with normalization of CBF. To study the effects of alterations of CBF on the development of brain edema, we administered intravenous (IV) indomethacin to rats receiving an ammonia infusion after portacaval anastomosis. This model predictably develops brain edema and a marked increase in CBF at 3 hours of infusion. Brain water was measured with the gravimetry technique; CBF was monitored with both laser Doppler flowmetry and radioactive microspheres, whereas intracranial pressure (ICP) was monitored with a cisterna magna catheter. Coadministration of indomethacin prevented the increase in CBF seen with ammonia alone (110 +/- 19% vs. -2 +/- 9%) as well as the increase in brain water (80.86 +/- 0.12% vs. 80.18 +/- 0.06%) and the increase in ICP. Plasma ammonia and brain glutamine levels were markedly elevated in the ammonia-infused group and unaffected by indomethacin. However, ammonia uptake by the brain was significantly reduced by indomethacin. Levels of 6-keto-PGF(1alpha), a stable metabolite of prostacyclin, were reduced in the cerebrospinal fluid (CSF) of indomethacin-treated animals. As with mild hypothermia, avoiding cerebral vasodilatation with indomethacin will prevent the development of brain edema in this hyperammonemic model. Cerebral vasoconstriction reduces cerebral ammonia uptake and, if selective to the brain, may be of benefit in FHF.
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PMID:Indomethacin prevents the development of experimental ammonia-induced brain edema in rats after portacaval anastomosis. 1148 8

Some stroke patients suffering acute middle cerebral artery (MCA) infarction develop massive brain edema and herniation, a condition known as malignant MCA infarction. Severe swelling increases intracranial pressure (ICP) and leads to progressive brainstem dysfunction. Once ICP reaches critical values (>30 mm Hg) herniation occurs, usually within 2 to 5 days. Patients rarely survive (80% mortality) with standard treatment, and those who do are often severely disabled. Malignant MCA infarction is often missed by neurologists, despite well-defined clinical and neuroimaging (CT scan) diagnostic criteria. After diagnosis, conventional treatments such as osmotherapy, barbiturates, buffers, and hyperventilation center on reducing ICP. The goal of hyperosmolar therapy is to increase the serum osmolarity to approximately 315-320 mOsm/L. Enteric glycerol is used routinely to reduce ICP. In more severe cases and when glycerol fails, mannitol may be administered. Other therapies are also available, including hypertonic saline solution, THAM (Tris-hydroxy-methyl-aminomethane) buffer, and high-dose barbiturates. Hyperventilation also helps reduce ICP. All measures work effectively for a short time only. Other approaches to control elevated ICP, including decompression surgery and hypothermia, have shown promising results. In the Heidelberg decompression surgery trial, mortality in surgically treated patients was significantly lower (32%) than in non-treated patients (76%) despite conventional treatment. Importantly, of the surviving treated patients, 66% were rated independent with only mild to moderate disability. Moderate hypothermia (33-36 degrees C) has recently been shown to be effective in severe MCA infarction. Hypothermia induction within 14 hours of ischemic injury and maintained for 72 hours significantly reduced ICP and mortality (44%).
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PMID:Treatment options for large hemispheric stroke. 1155 58


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