Therapeutic hypothermia and temperature management
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Ther Hypothermia Temp Manag · Jun 2018
Observational StudyPlasma Neutrophil Gelatinase-Associated Lipocalin Measured Immediately After Restoration of Spontaneous Circulation Predicts Acute Kidney Injury in Cardiac Arrest Survivors Who Underwent Therapeutic Hypothermia.
Early diagnosis of acute kidney injury (AKI) after cardiac arrest (CA) is challenging. We aimed to identify the diagnostic and prognostic performance of neutrophil gelatinase-associated lipocalin (NGAL) for AKI and its clinical outcomes. A retrospective observational study, involving adult comatose CA survivors treated with therapeutic hypothermia between May 2013 and December 2016, was conducted. ⋯ The development of AKI was independently associated with mortality (OR 4.926; 95% CI 2.353-10.311); however, NGAL level was not associated with mortality (OR 1.000; 95% CI 0.999-1.001). Plasma NGAL level measured after ROSC can be an early predictor for the development of AKI after CA. The presence of AKI was associated with increased inhospital mortality.
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Ther Hypothermia Temp Manag · Jun 2018
Determination of the Target Temperature Required to Block Increases in Extracellular Glutamate Levels During Intraischemic Hypothermia.
This study aimed to determine a target temperature for intraischemic hypothermia that can block increases in extracellular glutamate levels. Two groups of 10 rats each formed the normothermia and intraischemic hypothermia groups. Extracellular glutamate levels, the extracellular potential, and the cerebral blood flow were measured at the adjacent site in the right parietal cerebral cortex. ⋯ In conclusion, the target temperature for blocking glutamate release during intraischemic hypothermia was found to be 32.6°C ± 0.9°C. Our results suggest that the induction of intraischemic hypothermia can maintain low glutamate levels without disrupting glutamate reuptake. Institutional protocol number: OKU-2016146.
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Ther Hypothermia Temp Manag · Jun 2018
Precise Control of Target Temperature Using N6-Cyclohexyladenosine and Real-Time Control of Surface Temperature.
Targeted temperature management is standard of care for cardiac arrest and is in clinical trials for stroke. N6-cyclohexyladenosine (CHA), an A1 adenosine receptor (A1AR) agonist, inhibits thermogenesis and induces onset of hibernation in hibernating species. Despite promising thermolytic efficacy of CHA, prior work has failed to achieve and maintain a prescribed target core body temperature (Tb) between 32°C and 34°C for 24 hours. ⋯ All animals treated in this way rewarmed without incident. During the initiation of cooling, we observed bradycardia within 30 minutes of the start of IV infusion, transient hyperglycemia, and a mild hypercapnia; the latter normalized via metabolic compensation. In conclusion, we describe an intravenous delivery protocol for CHA at 0.25 mg/(kg·h) that, when coupled with conductive cooling, achieves and maintains a prescribed and consistent target Tb between 32°C and 34°C for 24 hours.