Cerebral oxidative metabolism failure in traumatic brain injury: “Brain shock”

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• 作者：Christos Lazaridis ; MD ; ^{lazaridi@bcm.edu}
• 关键词：Hypoxia ; Blood flow ; Intracranial pressure ; Oxygen metabolic rate ; Mitochondria ; Tissue oxygen tension
• 刊名：Journal of Critical Care
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：37
• 期：Complete
• 页码：230-233
• 全文大小：202 K
• 卷排序：37

文摘

Shock is a systemic form of acute circulatory failure leading to cellular dysoxia and death. Such a state of aerobic metabolism failure also underlies neuronal cell death in severe traumatic brain injury. It is becoming increasingly recognized that ischemic hypoxia is not the sole mechanism and that multiple alternate cooperating mechanisms may be responsible for compromising neuronal oxidative metabolism. These different mechanisms can be usefully understood via analysis of the classic subdivisions of tissue hypoxia. This approach could lead to an alternative treatment paradigm toward cerebral oxygen metabolic rate targeting instead of the traditional targets of intracranial and perfusion pressures.