Brain Resuscitation: Yesterday, Today and Tomorrow

  • Bo K. Siesjö
  • Maj-Lis Smith


It is common knowledge that brain cells, notably neurons, are very sensitive to oxygen deprivation. Several decades ago, the prevailing dogma was that brain cells could tolerate anoxia for only 3–4 min. This concept was based on both clinical experience and on several experimental studies in which the circulation to the brain was temporarily arrested. The experience of clinicians attempting to resuscitate patients after cardiac arrest is exemplified by the title of an article published more than 30 years ago, which stated that brain damage was incurred following cardiac arrest of more than 4 min duration [1]. Some previous experimental studies [2], were in agreement with these clinical findings revealing clear evidence of brain damage in animals with transient ischemia lasting longer than 4–5 min. However, experimental work conducted in the period around 1960 by Hirsch, Schneider, and their collaborators indicated the likelihood that such short revival times reflected the susceptibility of the heart to anoxia, rather than the brain [3,4]. The revival times were then defined as the longest ischemic periods which the brain could tolerate without functional or structural damage. Thus, when Hirsch et al. took precautions to protect the heart against anoxic damage, the revival times rose to 8–10 min at temperatures of around 37°C. They established that resuscitation of the brain was optimal only if the perfusion pressure of the brain could be promptly restored at the termination of the ischemia. This finding seemed to provide an explanation for the short revival periods following cardiac arrest, a condition in which post-ischemic blood pressure is often suboptimal. As a result, the findings inspired both clinical and experimental workers to raise postischemic perfusion pressure by the administration of pressure agents, such as catecholamines. When these principles were adopted, revival times for recovery of neurological function in experimental ischemia were prolonged, sometimes to 10–12 min [5,6], and in some conditions, even longer. However, it is possible that accidental hypothermia could have contributed to the most dramatic results.


Ischemic Damage Brain Damage NMDA Antagonist Cereb Blood Flow Ischemic Brain Damage 
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Copyright information

© Springer-Verlag Tokyo 1991

Authors and Affiliations

  • Bo K. Siesjö
  • Maj-Lis Smith
    • 1
  1. 1.Laboratory of Experimental Brain Research, Forskningsavd 4Lund University Hospital85 LundSweden

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