Brain Oxygenation and Energy Metabolism: Part I???Biological Function and Pathophysiology

Abstract

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.

Outcome following decompressive craniectomy for malignant swelling due to severe head injury

“…Mechanoporation, ischemia, and energy failure at the level of mitochondria are some of the causes of ionic and neurochemical cascades contributing to cytotoxic brain edema and intracranial hypertension resistant to maximal medical management. 7,8,[12][13][14]17,23,30,58,71,72,74,91,92,99,115,118,124 Adherence to published prehospital, intensive care, and surgical guidelines for the management of severe head injury has lessened the burden of hypotension or hypoxia and has mitigated deleterious effects of increased ICP due to brain swelling; 4,6,18,22,43,76,79 nevertheless, straightforward correction of pathophysiological pathways and neurochemical cascades has not been easy. Translational research on severe head injury has revealed no easy pharmaceutical therapy for severe head injury and cerebral swelling.…”

Oxygen, a Key Factor Regulating Cell Behavior during Neurogenesis and Cerebral Diseases

“…Tissue hypoxia-induced by brain insults plays a critical role in the primary and secondary events leading to cell death after cerebral ischemia (Zauner et al, 2002). Therefore, improving brain tissue oxygenation is a logical and important strategy of stroke treatment to delay the transition of ischemia to infarction (“buying time”).…”

Oxidative stress and apoptosis after acute respiratory hypoxia and reoxygenation in rat brain

“…Hypoxia modifies the activity of the cytochrome chain responsible for mitochondrial oxidative phosphorylation, resulting in a decrease in ATP synthesis and increased ROS [9] at the same time as a decrease in the activity of the cellular antioxidant system [5], [10], which may lead to oxidative stress. The brain is particularly vulnerable to the effects of ROS for several reasons: (a) it has a low catalase and glutathione peroxidase activity [11], (b) it is rich in lipids with unsaturated fatty acids that can react with ROS and generate peroxyl radicals that oxidize the lipid membrane [12], (c) it has a high metabolic activity and high oxygen consumption [13].…”