Abstract
The clinical treatment of brain-injured patients has been previously based on information derived from experimental animal studies concerning brain trauma, ischemia, infarction, hypoxia, and cardiac arrest [9]. However, the differences between species from animal to human, including differences in pathophysiology of severely brain-injured patients and experimental animal models, are not absolutely clear. One difference in brain injury mechanism is the effect of anesthesia. The direct brain injury mechanisms such as necrosis, ischemia, brain edema, intracranial pressure (ICP) elevation, and nonspecific brain damage caused by neuroexcitation apoptosis are not so different between clinical patient s and experimental animal models [1,5,10,11]. However, systemic stress reaction is more severe in patients than in experimental animal models, because stress-associated neurohormonal reaction is limited under anesthesia. In experimental animal studies, harmful stress-associated neurohormonal reactions caused by stimulation of the hypothalamus-pituitary- adrenal (HPA) [2,3] and hypothalamus-pituitary- thyroid axis are prevent ed by anesthesia.
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Hayashi, N., Dietrich, D.W. (2004). The Difference in Brain Injury Mechanism in Experimental Laboratory Models and Human Patients. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_26
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DOI: https://doi.org/10.1007/978-4-431-53953-7_26
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