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

Sheep cold stressed for 10.5 h had plastic coats applied then the cold stress was continued. In 9 of 10 sheep (test group) showing hypothermia at the time coats were applied, body temperatures had returned to near normal 2.5 h later and to normal in 13.5 h. One sheep severely hypothermic before the coat was applied did not improve and was killed after 2.5 h. Sheep that were cold stressed without coats (wet controls) developed marked hypothermia and were killed between 10.5 h and 21 h. Rectal temperatures remained normal in controls that were cold stressed with coats on (coated wet controls) and in the controls not subjected to wetting (dry controls). Plasma cortisol increased markedly in the cold stressed sheep until plastic coats were applied, but the levels had fallen to normal levels 20 h later. Serum thyroxine levels increased at a faster rate in the test group and in wet controls than in the dry controls and coated wet controls during the first 9 h of cold stress. In 4 sheep of the test group energy utilisation increased markedly and remained high for a variable time after coats were applied then gradually returned to pre-cold stress levels. Liver tyrosine aminotransferase levels of the wet controls were markedly elevated compared to levels found in the test group sheep killed 79.5 h after coats were applied. Histological changes in the spleen and liver of wet controls was absent or only mildly present in the test group sheep. There was severe depletion of muscle and liver glycogen in the wet controls compared with the test group sheep, which were similar to the dry controls and coated wet controls.
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PMID:Protection of recently shorn sheep against adverse weather using plastic coats. 405 11

Hypothermic preservation of hepatocytes on gelatin gels allows hepatocytes to be stored for at least 9 days. The procedure is easy, inexpensive and does not require specialised equipment. The cells retain their morphology and are released as separate spherical entities by dissolving the gelatin layer at 37 degrees. The recovered cells have an intact plasma membrane as judged by lactate dehydrogenase activity, attachment efficiency and subsequent monolayer formation in culture. Functional tests show that the cells recover quickly from the storage conditions. Rates of protein synthesis are maintained over a 6 day period and remain at 62% of the initial level on day 9. The liver specific, hormonal induction of the enzyme tyrosine aminotransferase is apparent throughout the culture period. In addition a phenotypic marker enzyme, gamma-glutamyl transpeptidase, remained at basal levels.
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PMID:Hypothermic preservation of hepatocytes on gelatin gels. 789 93

Upon intravenous injection of tumour necrosis factor (TNF) in mice, a systemic inflammatory response syndrome (SIRS) is initiated, characterized by an acute cytokine storm and induction of vascular hyperpermeability. Connexin43 hemichannels have been implicated in various pathological conditions, e.g. ischemia and inflammation, and can lead to detrimental cellular outcomes. Here, we explored whether targeting connexin43 hemichannels could alleviate TNF-induced endothelial barrier dysfunction and lethality in SIRS. Therefore, we verified whether administration of connexin43-targeting-peptides affected survival, body temperature and vascular permeability in vivo. In vitro, TNF-effects on connexin43 hemichannel function were investigated by single-channel studies and Ca2+-imaging. Blocking connexin43 hemichannels with TAT-Gap19 protected mice against TNF-induced mortality, hypothermia and vascular leakage, while enhancing connexin43 hemichannel function with TAT-CT9 provoked opposite sensitizing effects. In vitro patch-clamp studies revealed that TNF acutely activated connexin43 hemichannel opening in endothelial cells, which was promoted by CT9, and inhibited by Gap19 and intracellular Ca2+-buffering. In vivo experiments aimed at buffering intracellular Ca2+, and pharmacologically targeting Ca2+/calmodulin-dependent protein kinase-II, a known modulator of endothelial barrier integrity, demonstrated their involvement in permeability alterations. Our results demonstrate significant benefits of inhibiting connexin43 hemichannels to counteract TNF-induced SIRS-associated vascular permeability and lethality.
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PMID:Blocking connexin43 hemichannels protects mice against tumour necrosis factor-induced inflammatory shock. 3171 98