Abstract
A recent clinical trial of brain hypothermia for postresuscitation management of cardiopulmonary arrest (CPA) patients demonstrated the effectiveness of the treatment [3,14,17,18]. The concept and mechanism of hypothermia are similar to those in experimental animal studies, such as the prevention of brain edema and free radical reactions after reperfusion, and management of brain hypoxia [2,3,17,20,21]. However, the brain injury mechanism after cardiac arrest in humans is not similar to that in anesthetized experimental animal models [7,8,13]. Stress to the hypothalamuspituitary- adrenal (HPA) axis [4] and excess neurohormonal reactions [15,16] after cardiac arrest produces brain injury mechanisms that were not observed in anesthetized experimental animal models [11,12]. Insulin-resistant hyperglycemia associated with epinephrine surge [7,9–11] and slow release of bound oxygen from hemoglobin [5,11] that produces ineffective oxygen inhalation are major issues at the acute stage after resuscitation from cardiac arrest (Fig. 107).
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Hayashi, N., Dietrich, D.W. (2004). Brain Hypothermia After Resuscitation from Cardiopulmonary Arrest. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_56
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DOI: https://doi.org/10.1007/978-4-431-53953-7_56
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