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

Perinatal hypoxic-ischaemic brain damage is an important cause of neonatal death and permanent neurological impairment. Therapeutic hypothermia may reduce the development of brain damage after hypoxia. Whether to use room-air or 100% oxygen for resuscitation of the asphyxiated neonate is still debated, and there is little knowledge about the combined effects of therapeutic hypothermia and room air resuscitation. We used human NT2-N neurons to test whether oxygen level during reoxygenation would influence the protective effect of hypothermia. Oxygen-glucose deprived (OGD) human NT2-N neurons were exposed to 20 min of low (1%), medium (21%) or high (95%) oxygen concentrations immediately after hypoxia, followed by 20.5 h of hypothermia (33 degrees C) or normothermia (37 degrees C). Cell viability was determined by a methyltetrazolium assay (MTT), cellular energy failure by hypoxanthine release to supernatant, and inflammatory response by the release of IL-8 (Interleukin-8), bFGF (basic fibroblast growth factor), IP-10 (interferon-inducible protein-10) and MCP-1 (monocyte chemotactic protein-1) to supernatant. Post-hypoxic hypothermia resulted in significantly higher MTT cleavage (average 27% of control (SD 11%) vs 24% (SD 12%), p=0.005). Hypoxanthine release was increased both immediately after hypoxia and 21 h later, however less in hypothermic (median increase 2.0 mumol/L, IQR 1.2-3.2) compared to normothermic cells (2.7 mumol/L, IQR 2.1-4.1, p<0.05). All four inflammatory markers increased after hypoxia but not differently between normothermic and hypothermic cells. Oxygen level had no significant effect on cell viability, inflammatory markers or energy status, irrespective of temperature level. We conclude that hypothermia protects isolated neurons after in vitro hypoxia, and that this protection is not affected by hyperoxic, normoxic or hypoxic reoxygenation.
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PMID:Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation. 1914 35

Despite the widespread interest in the clinical applications of hypothermia, the cellular mechanisms of hypothermia-induced neuroprotection have not yet been clearly understood. Therefore, the aim of this study was to elucidate the cellular effects of clinically relevant hypothermia and rewarming on the morphological and functional characteristics of microglia. Microglial cells were exposed to a dynamic cooling and rewarming protocol. For stimulation, microglial cells were treated with 1 microg/mL lipopolysaccharide (LPS). We found that hypothermia led to morphological changes from ramified to ameboid cell shapes. At 2 h after hypothermia and rewarming, microglial cells were again ramified with extended branches. Moreover, we found enhanced cell activation after rewarming, accompanied by increased phagocytosis and adenosine triphosphate consumption. Interestingly, hypothermia and rewarming led to a time-dependent significant up-regulation of the anti-inflammatory cytokines interleukin-10 and interleukin-1 receptor antagonist in stimulated microglial cells. This is in line with the reduced proliferation and time-dependent down-regulation of the pro-inflammatory cytokines tumor necrosis factor-alpha and monocyte chemotactic protein-1 in comparison to normothermic control cells after LPS stimulation. Furthermore, degradation of the inhibitor of the nuclear transcription factor-kappaB (IkappaB-alpha) was diminished and delayed under conditions of cooling and rewarming in LPS-stimulated microglial cells. Thus, our results show that hypothermia and rewarming activate microglial cells, increase phagocytosis and shift the balance of cytokine release in stimulated microglial cells towards the anti-inflammatory cytokines. This could be a new cellular mechanism of hypothermia-induced neuroprotection mediated by activated microglial cells.
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PMID:Mechanisms of hypothermia-induced cell protection mediated by microglial cells in vitro. 2037 79