anoxic coma
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Resuscitation ◽  
2021 ◽  
Vol 167 ◽  
pp. 430-431 ◽  
Author(s):  
Maenia Scarpino ◽  
Antonello Grippo ◽  
Claudio Sandroni
Keyword(s):  

2021 ◽  
Vol 7 ◽  
pp. 100151
Author(s):  
Patrick J. Coppler ◽  
Amanda E. Kusztos ◽  
Mark Andreae ◽  
Brad W. Butcher ◽  
Ankur Doshi ◽  
...  

Author(s):  
Thijs M. van Soest ◽  
Anne-Fleur van Rootselaar ◽  
Marjolein M. Admiraal ◽  
Wouter V. Potters ◽  
Johannes H.M.T. Koelman ◽  
...  
Keyword(s):  

2020 ◽  
Vol 124 (6) ◽  
pp. 1754-1765
Author(s):  
Rachel A. Van Dusen ◽  
Hannah Shuster-Hyman ◽  
R. Meldrum Robertson

We demonstrate the involvement of ATP-sensitive K+ (KATP) channels during recovery from spreading depolarization (SD) induced via anoxic coma in locusts. KATP inhibition using glybenclamide impaired ion homeostasis across the blood-brain barrier, resulting in a longer time to recovery of transperineurial potential following SD. Comparison with ouabain indicates that the effects of glybenclamide are not mediated by the Na+/K+-ATPase but are a result of KATP channel inhibition.


2020 ◽  
Vol 124 ◽  
pp. 104057 ◽  
Author(s):  
Rachel A. Van Dusen ◽  
Christopher Lanz ◽  
R. Meldrum Robertson

2020 ◽  
Vol 48 (8) ◽  
pp. e639-e647 ◽  
Author(s):  
Patrice Peran ◽  
Briguitta Malagurski ◽  
Federico Nemmi ◽  
Benjamine Sarton ◽  
Hélène Vinour ◽  
...  

2019 ◽  
Author(s):  
Rachel A. Van Dusen ◽  
Christopher Lanz ◽  
R. Meldrum Robertson

AbstractWhen exposed to prolonged anoxia insects enter a reversible coma during which neural and muscular systems temporarily shut down. Nervous system shut down is a result of spreading depolarization throughout neurons and glial cells. Upon return to normoxia, recovery occurs following the restoration of ion gradients. However, there is a delay in the functional recovery of synaptic transmission following membrane repolarization. In mammals, the build-up of extracellular adenosine following spreading depolarization contributes to this delay. Adenosine accumulation is a marker of metabolic stress and it has many downstream effects through the activation of adenosine receptors. Here we demonstrate that adenosine lengthens the time to functional recovery following anoxic coma in locusts. Caffeine, used as an adenosine receptor antagonist, decreased the time to recovery in intact animals and lengthened the time to recovery in semi-intact animals. Our results show that the rate of recovery in insect systems is affected by the presence of adenosine.


2019 ◽  
Vol 130 (7) ◽  
pp. e40-e41
Author(s):  
Rubjona Xhani ◽  
Simone Beretta ◽  
Anna Coppo ◽  
Elisa Bianchi ◽  
Clara Zanchi ◽  
...  

2019 ◽  
Author(s):  
A. Floyrac ◽  
A. Doumergue ◽  
N. Kubis ◽  
D. Holcman

AbstractThe severity of neuronal damages in comatose patients following anoxic brain injury can be probed by evoked auditory responses. However, it remains challenging to predict the return to full consciousness of post-anoxic coma of hospitalized patients. We presented here a method to predict the return to consciousness based on the analysis of periodic responses to auditory stimulations, recorded from surface cranial electrodes. The input data are event-related potentials (ERPs), recorded non-invasively with electro-encephalography (EEG). We extracted several novel features from the time series responses in a window of few hundreds of milliseconds from deviant and non-deviant auditory stimulations. We use these features to construct two-dimensional statistical maps, that show two separated clusters for recovered (conscience) and deceased patients, leading to a high classification success as tested by a cross-validation procedure. Finally, using Gaussian, K-neighborhood and SVM classifiers, we construct probabilistic maps to predict the outcome of post-anoxic coma. To conclude, statistics of deviant and non-deviant responses considered separately provide complementary and confirmatory predictions for the outcome of anoxic coma.


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