title: Individual value of brain tissue oxygen pressure, microvascular oxygen saturation, cytochrome redox level, and energy metabolites in detecting critically reduced cerebral energy state during acute changes in global cerebral perfusion.
abstract: The authors assessed the diagnostic value of brain tissue oxygen tension (PbrO2), microvascular oxygen saturation (SmvO2), cytochrome oxidase redox level (Cyt a+a3 oxidation), and cerebral energy metabolite concentrations in detecting acute critical impairment of cerebral energy homeostasis. Each single parameter as well as derived multimodal indices (arteriovenous difference in oxygen content [AVDO2], cerebral metabolic rate for oxygen [CMRO2], fractional microvascular oxygen extraction [OEF]) were investigated during controlled variation of global cerebral perfusion using a cisternal infusion technique in 16 rabbits. The objective of this study was to determine whether acute changes between normal, moderately, and critically reduced cerebral perfusion as well as frank ischemia defined by local cortical blood flow (lcoBF), brain electrical activity (BEA), and brain stem vasomotor control can be reliably identified by SmvO2, PbrO2, Cyt a+a3 oxidation, or energy metabolites (glutamate, lactate/pyruvate ratio). PbrO2, SmvO2, and Cyt a+a3 oxidation, but not cerebral perfusion pressure, were closely linked to lcoBF and BEA and allowed discrimination between normal, moderately reduced, and critically reduced cerebral perfusion (P < 0.01). Glutamate concentrations and the lactate/pyruvate ratio varied significantly only between moderately reduced cerebral perfusion and frank ischemia (complete loss of BEA and brain stem vasomotor control). Therefore, PbrO2, SmvO2, and Cyt a+a3 oxidation, but not glutamate and the lactate/pyruvate ratio, reliably predict the transition from moderately to critically reduced cerebral perfusion with impending energy failure.
authors.affiliation: Department of Neurosurgery, University of Freiburg, Freiburg, Germany. scheufle@nz11.ukl.uni-freiburg.de
authors.forename: Kai-Michael
authors.initials: KM
authors.lastname: Scheufler
authors.forename: Ariane
authors.initials: A
authors.lastname: Lehnert
authors.forename: Hans-Joachim
authors.initials: HJ
authors.lastname: Rohrborn
authors.forename: Joachim
authors.initials: J
authors.lastname: Nadstawek
authors.forename: Christof
authors.initials: C
authors.lastname: Thees
mesh_terms: D000465:Algorithms; D000818:Animals; D001923:Brain Chemistry / Q000502:physiology*; D002545:Brain Ischemia / Q000503:physiopathology; D001933:Brain Stem / Q000502:physiology; D002196:Capillaries / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002946:Cisterna Magna; D003580:Cytochromes / Q000378:metabolism*; D045264:Cytochromes a / Q000378:metabolism; D045266:Cytochromes a3 / Q000378:metabolism; D004594:Electrophysiology; D004734:Energy Metabolism / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism; D007262:Infusions, Intravenous; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D010084:Oxidation-Reduction; D010092:Oximetry; D010101:Oxygen Consumption / Q000502:physiology*; D011048:Polarography; D019289:Pyruvic Acid / Q000378:metabolism; D011817:Rabbits
chemical_list: D003580:Cytochromes; D045266:Cytochromes a3; D019344:Lactic Acid; D018698:Glutamic Acid; D019289:Pyruvic Acid; D045264:Cytochromes a