Brain oxygenation and energy metabolism: part I-biological function and pathophysiology.
CONTINUOUS OXYGEN DELIVERY and CO(2) clearance are paramount in the maintenance of normal brain function and tissue integrity. Under normal conditions, aerobic metabolism is the major source of energy in the brain, but this system may be compromised by the interruption of substrate delivery and disturbances in cerebral metabolism. These disruptions are major factors contributing to ischemic and hypoxic brain damage resulting from traumatic brain injury, stroke, and subarachnoid hemorrhage. There is evidence that mitochondrial function also is reduced after injury. Furthermore, early impairment of cerebral blood flow in patients with severe injury correlates with poor tissue oxygenation and may be an important parameter in secondary damage. Recent advances in brain tissue monitoring in the intensive care unit and operating room have made it possible to continuously measure tissue oxygen tension and temperature, as well as certain aspects of brain metabolism and neurochemistry. Therefore, it is important to understand the physiological process and the pathophysiology produced by these events. This is Part I of a two-part review that analyzes the physiology of cerebral oxygenation and metabolism as well as some of the pathological mechanisms involved in ischemic and traumatic brain injuries. Brain tissue monitoring techniques will be examined in the second article of this two-part series. To understand cerebral oxygenation, it is important to understand cerebral blood flow, energy production, ischemia, acidosis, generation of reactive oxygen species, and mitochondrial failure. These issues provide the basis of knowledge regarding brain bioenergetics and are important topics to understand when developing new approaches to patient care.
Division of Neurosurgery, Medical College of Virginia, USA. Azauner@mednet.ucla.edu
Alois
A
Zauner
Wilson P
WP
Daugherty
M Ross
MR
Bullock
David S
DS
Warner
D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008928:Mitochondria / Q000502:physiology; D010101:Oxygen Consumption