Resuscitation
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Randomized Controlled Trial
Impaired β-adrenergic receptor signalling in post-resuscitation myocardial dysfunction.
Post-resuscitation myocardial dysfunction is a major cause of fatality in patients receiving successful cardiopulmonary resuscitation. The mechanism of post-resuscitation myocardial dysfunction is largely unknown, although is generally considered related to ischaemia occurring during cardiac arrest and resuscitation and/or reperfusion injury after restoration of circulation. A key mechanism responsible for reduced contractile reserves in chronic heart failure is impaired β-adrenergic receptor signalling. Thus, we hypothesised that β-adrenergic receptor signalling is markedly abnormal in the post-resuscitation period following cardiopulmonary resuscitation. ⋯ β-Adrenergic receptor signalling is markedly impaired in the post-resuscitation period, which may be a mechanism of post-resuscitation myocardial dysfunction.
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Randomized Controlled Trial
Effects of continuous haemofiltration on serum enzyme concentrations, endotoxemia, homeostasis and survival in dogs with severe heat stroke.
To examine the effectiveness of continuous haemofiltration as a treatment for severe heat stroke in dogs. ⋯ Continuous haemofiltration rapidly reduced body temperature, normalised haemodynamics and electrolytes, improved serum enzyme concentrations and increased survival in dogs with heat stroke. Continuous haemofiltration may be an effective treatment for heat stroke.
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Randomized Controlled Trial
Fluoxetine has neuroprotective effects after cardiac arrest and cardiopulmonary resuscitation in mouse.
Fluoxetine, a selective serotonin reuptake inhibitor, is protective in a rat focal ischaemia model via anti-inflammatory mechanisms. Cardiac arrest and cardiopulmonary resuscitation (CA/CPR) were performed in mice to test the hypothesis that fluoxetine protects the brain following global cerebral ischaemia, even when administered after an insult. ⋯ Our data showed that 10mg/kg fluoxetine administered following global cerebral ischaemia decreases neuronal damage. Although long-term neuroprotection needs further study, the results of our study suggest that fluoxetine may have therapeutic potential when administered after global cerebral ischaemia, cardiac arrest and cardiopulmonary resuscitation.