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)

The purpose of this study was to investigate the effects of temperature change on the coagulation time of blood at two different hematocrit levels by using various coagulation-monitoring devices. The devices used in this study were the Bayer Rapid Point Coag Analyzers, Hemochron Jr. Signature, Hemochron Response, Medtronic ACT II, and Haemoscope Thrombelastograph. One unit of human bank blood was used in this study. The hematocrit level was adjusted to 40% and 20%. A control bath and experimental bath were set up. Control blood was maintained at 37 degrees C and tested every 45 +/- 15 min throughout the experimental period of 6 h to demonstrate the stability of the model. The experimental blood was tested at temperature points of 37, 32, 27, 32, 37, 42, and 37 degrees C. Activated clotting time (ACT) tended to increase when the temperature was initially decreased from 37 to 27 degrees C, which reached a statistically significant level when measured by the Hemochron Response at both the 20% (147 +/- 10.7 to 159.3 +/- 11.0, p < .0332) and 40% hematocrit level (130 +/- 14.9 to 152.1 +/- 19.7, p < .0148). ACT was decreased significantly (p < .05) when the temperature was increased to 42 degrees C as measured by all machines except the Hemochron Jr. Signature at the 20% hematocrit level. ACT was significantly higher (p < .05) at a 20% hematocrit level as compared to that at a 40% hematocrit level on all devices for the majority of temperature points. These data suggested that hypothermia only increased ACT when measured by a macrosample device requiring a milliliter sample (Hemochron Response). However, hemodilution induced anticoagulatory effects and hyperthermia caused an acceleration in coagulation by all devices utilized in this study.
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PMID:Quantitative evaluation of hypothermia, hyperthermia, and hemodilution on coagulation. 1146 35

Considerable effort and substantial funding has gone towards the development of a neuroprotective agent that could be given after brain trauma to reduce mortality and improve functional recovery. There have been many failed or inconclusive studies to date. In Europe two promising studies have been stopped or shelved (Lubeluzole, Janssen-Cilag and BAYx3702, Bayer) and the future of pharmacological neuroprotection after traumatic brain injury is in doubt. Clinicians managing patients with a head injury are therefore left with the detection and prevention of secondary insults to the brain, including the management of medical complications of brain injury, and non-pharmaceutical interventions that might beneficially modify the brain's response to trauma. Of the potential interventions, moderate hypothermia is the most promising.
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PMID:Head injury: complications and management. 1701 60