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

To determine the ability of intraoperative hypothermia to modify changes in the plasma protein component of the acute-phase response (APR) and the plasma hormone component of the endocrine response (ER) to surgical injury, 20 patients undergoing coronary artery surgery were randomised to an intraoperative blood temperature of 28 degrees C or 20 degrees C during cardiopulmonary bypass (CPB). Serial measurements of pack-cell-volume corrected concentrations (PCVCC) of five plasma proteins (albumin, prealbumin, transferrin, caeruloplasmin, ferritin) and six plasma hormones (adrenaline, noradrenaline, cortisol, triiodothyronine, thyroxine, and thyroid-stimulating hormone) were obtained twice preoperatively, seven times during surgery, six times in the 24 hours following surgery, and a further four times until the seventh postoperative day. A more profound level of intraoperative hypothermia significantly reduced the plasma adrenaline response to CPB but not the other components of the ER or APR.
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PMID:The effects of systemic intraoperative hypothermia on the acute-phase and endocrine response to cardiac surgery. 163 76

In this study we investigated the effects of severe hypothermia (cryoinjury) on oligodendrocyte (OL) cell marker expression and morphological features. We used a chemically defined cell culture medium, glial development medium (GDM), which favored the optimal expression of the OL phenotype in CG4 cells. Experiments using CG4 cells cultured in 2% serum or in GDM were conducted in parallel. After severe hypothermia, cells were reanimated at 37 degrees C and 4.5% CO(2) and cultured in either GDM or in medium supplemented with 2% serum. In either medium, around 70% of the total number of cells detached within 2 to 4 hours following reanimation. Oligodendroglial markers such as A2B5, O4, Tf, ferritin, tubulin, and MBP were examined by double and triple immunofluorescence. All of these markers except MBP re-appeared at different times during the recovery period for up to 48 hours. Glial fibrillary acidic protein (GFAP) and heat shock protein 60 (HSP-60) were used as injury markers. The presence of serum induced HSP-60 expression, while GDM did not. All CG4 cells expressed HSP-60 in response to hypothermia independently of the cell culture medium used. Cryoinjury induced a spectrum of morphological changes in CG4 cells. The expression of OL specific markers was also influenced by hypothermia. Moreover both, serum and cryoinjury induced the expression of HSP-60 that colocalized with OL and myelin markers. The expression of GFAP by injured cells but not by normal cells corroborated the state of injury of CG4 cells.
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PMID:In vitro injury model for oligodendrocytes: development, injury, and recovery. 1127 24

In asphyxiated newborns, iron, released from heme and ferritin and deposited in the brain, contributes to neurodegeneration. Because hypothermia provides neuroprotection, newborn mammals, showing reduced body temperature, might avoid iron-mediated neurotoxicity. However, hypothermia leads to acidosis, which induces hyperferremia. Therefore, we decided to study the effects of body temperature on plasma pH and iron levels in newborn rats exposed to a critical anoxia. Rectal temperature was kept at 33 degrees C (typical of neonates), reduced by 2 degrees C, or elevated to a level typical of healthy (37 degrees C) or febrile (39 degrees C) adults. Arterial blood samples were collected at 0, 10, 20, 30, and 120 min postanoxia. Control samples were obtained from normoxic, temperature-matched neonates. Anoxia tolerance time decreased progressively at rectal temperatures exceeding 33 degrees C. Neither pH nor plasma iron were significantly affected by anoxia at 33 degrees C. Although hypothermia (31 degrees C) resulted in acidosis in normoxic rats, both pH and iron levels were hardly influenced by anoxia. However, acidosis and hyperferremia, proportional to body temperature, developed at 37 and 39 degrees C. In conclusion, reduced body temperature is likely to protect asphyxiated newborns against iron-mediated brain injury.
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PMID:Effect of temperature on postanoxic, potentially neurotoxic changes of plasma pH and free iron level in newborn rats. 1147 Mar 28

In asphyxiated newborns iron, released from heme and ferritin and deposited in the brain, contributes to neurodegeneration. Because hypothermia provides neuroprotection, newborn mammals, showing spontaneously reduced body temperature, might avoid the iron-mediated neurotoxicity. Therefore, we decided to study the effects of body temperature and chelation of iron with deferoxamine on iron accumulation in the brain of three weeks old rats exposed neonatally to a critical anoxia. At the age of two days, newborn rats were exposed to anoxia in 100% nitrogen atmosphere. Rectal temperature was kept at 33 degrees C (typical of the rat neonates), or elevated to a level typical of febrile (39 degrees C) adults. Control rats were exposed to atmospheric air in the respective thermal conditions. Half of the rats exposed to anoxia under hyperthermic conditions were injected with deferoxamine (DF), immediately after anoxia and 24 h later. Regional changes in cerebral iron deposition were examined in the frontal cortex, the hippocampus and the striatum, using iron histochemistry, when the rats reached the age of three weeks. Increased iron staining was found in neurons of each of the three cerebral regions in rats exposed to neonatal anoxia under hyperthermic conditions and the iron accumulation was prevented by postanoxic DF injection. In conclusion, febrile body temperature amplifies cerebral hyperferremia, which might induce neurodegenerative disturbances in the brain. On the other hand, a protection against the brain hyperferremia can be achieved by both the reduced physiological neonatal body temperature and by postasphyxic DF administration.
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PMID:Effect of neonatal body temperature on postanoxic, potentially neurotoxic iron accumulation in the rat brain. 1628 21

Hypothermia for myocardial protection or storage of vascular grafts may damage the endothelium and impair vascular function upon reperfusion/rewarming. Catalytic iron pools and oxidative stress are important mediators of cold-induced endothelial injury. Because endothelial cells are highly adaptive, we hypothesized that hypothermic preconditioning (HPC) protects cells at 0 degrees C by a heme oxygenase-1 (HO-1) and ferritin-dependent mechanism. Storage of human coronary artery endothelial cells at 0 degrees C caused the release of lactate dehydrogenase, increases in bleomycin-detectible iron (BDI), and increases in the ratio of oxidized/reduced glutathione, signifying oxidative stress. Hypoxia increased injury at 0 degrees C but did not increase BDI or oxidative stress further. HPC at 25 degrees C for 15-72 h attenuated these changes by an amount achievable by pretreating cells with 10-20 microM deferoxamine, an iron chelator, and protected cell viability. Treating cells with hemin chloride at 37 degrees C transiently increased intracellular heme, HO-1, BDI, and ferritin. Elevated heme/iron sensitized cells to 0 degrees C but ferritin was protective. HPC increased iron maximally after 2 h at 25 degrees C and ferritin levels peaked after 15 h. HO-1 was not induced. When HPC-mediated increases in ferritin were blocked by deferoxamine, protection at 0 degrees C was diminished. We conclude that HPC-mediated endothelial protection from hypothermic injury is an iron- and ferritin-dependent process.
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PMID:Hypothermic preconditioning of endothelial cells attenuates cold-induced injury by a ferritin-dependent process. 1913 23

We reported a girl with HHV-6 infection associated with both acute encephalopathy with biphasic seizures and late reduced diffusion, and hemophagocytic syndrome. She had a prolonged convulsion after a one-day history of febrile illness. Cerebrospinal fluid or brain CT showed no abnormalities on admission and her consciousness was recovered on the next day. However, a prolonged seizure and deterioration of consciousness appeared on the sixth day of illness. Diffusion-weighted images revealed marked reduction of water diffusion in the bilateral frontal areas. HHV-6 infection was virologically proven by polymerase chain reaction. She was treated with gamma-globulin, steroid pulse therapy, and brain hypothermia. In addition, decrease in white blood cells and platelet counts, and elevation of liver enzymes and ferritin were noted on the fourth day of illness. Hemophagocytic macrophages were revealed by bone marrow aspiration on the sixth day. Her hematological and blood chemistry abnormalities recovered gradually after steroid pulse therapy. An elevation of interleukin-6, -8, and -10, and tumor necrosis factor in the serum and that of interleukin-4, -6, and-8 in the cerebrospinal fluid were observed at the onset of a late seizure. These facts suggested that hypercytokinemia will be related to the pathogenesis of acute encephalopathy of our patient.
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PMID:Acute encephalopathy with biphasic seizures and late reduced diffusion associated with hemophagocytic syndrome. 1955 82