title: Cerebral oxidative metabolism failure in traumatic brain injury: "Brain shock".
abstract: 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.
authors: Division of Neurocritical Care and Vascular Neurology, Baylor College of Medicine, Houston, TX. Electronic address: lazaridi@bcm.edu.
authors: Christos
authors: C
authors: Lazaridis
mesh_terms: D001921:Brain / Q000378:metabolism*; D000070642:Brain Injuries, Traumatic / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D006801:Humans; D000860:Hypoxia / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D012769:Shock / Q000378:metabolism*
chemical_list: D010100:Oxygen
keywords: Blood flow; Hypoxia; Intracranial pressure; Mitochondria; Oxygen metabolic rate; Tissue oxygen tension