THE DEVELOPMENT of effective therapy to preserve normal neurological function in patients surviving a cardiac arrest hinges on our growing understanding of the pathophysiology of ischemic anoxia. It is worthwhile, then, to review our new understanding of these mechanisms, as well as the laboratory search for therapies to protect neurons injured by cardiac arrest.
The early doctrine that four to six minutes of ischemic anoxia leads to irreversible brain injury was based on work done in the 1940s with dogs subjected to breathing 100% nitrogen.1,2 However, it became apparent from work by Ames and Guarian3 and Hossman and Kleihues4 that the neurons themselves have substantial intrinsic resistance to complete ischemic anoxia. The evidence suggests that CNS neurons can tolerate between 20 and 60 minutes of complete ischemic anoxia without irreversible injury. Following these severe insults, neurons regain the ability to synthesize protein, produce adenosine triphosphate (ATP), and
White BC, Wiegenstein JG, Winegar CD. Brain Ischemic Anoxia: Mechanisms of Injury. JAMA. 1984;251(12):1586–1590. doi:10.1001/jama.1984.03340360052029
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