Editorial Views  |   April 2017
Anesthetic Neuroprotection? It’s Complicated
Author Notes
  • From the Multidisciplinary Neuroprotection Laboratories, Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina.
  • Accepted for publication January 4, 2017.
    Accepted for publication January 4, 2017.×
  • Corresponding article on page 653.
    Corresponding article on page 653.×
  • Address correspondence to Dr. Warner: david.warner@duke.edu
Article Information
Editorial Views / Central and Peripheral Nervous Systems
Editorial Views   |   April 2017
Anesthetic Neuroprotection? It’s Complicated
Anesthesiology 4 2017, Vol.126, 579-581. doi:10.1097/ALN.0000000000001535
Anesthesiology 4 2017, Vol.126, 579-581. doi:10.1097/ALN.0000000000001535
ANESTHETICS possess num -erous pharmacologic properties that could increase tolerance of brain to an ischemic insult. Despite investigation for over half a century,1  and robust demonstration of such benefit in laboratory animals,2  there is no solid evidence that anesthetic neuroprotection is present in humans.3  The article by Archer et al.4  in this issue of Anesthesiology provides considerable insight into this apparent paradox.
It once seemed so straight forward. The brain consumes adenosine triphosphate at an incredible rate and holds little stores of this critical metabolite. Hence, continuous delivery of oxygen and glucose is essential to maintain adenosine triphosphate synthesis, neural function, and cellular integrity. Most anesthetics can markedly suppress metabolic rate. Thus, the duration the brain can survive in low-flow or no-flow states should be increased substantially. Neuroprotection investigation was focused on the perioperative environment for several decades. Anesthesiologists and surgeons were at the forefront of therapeutic stroke research.
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