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Role of glucose-6-phosphate in cerebral dysfunction following hypoxia and hypotension.

Abstract
Rats were "stressed" by a 30-minute period of breathing 7.5% oxygen combined with hemorrhagic hypotension (x arterial pressure = 25 mm Hg), and then "resuscitated" by restoring the inspired oxygen concentration to 30% and reinfusing the blood previously removed to produce hypotension. We have previously noted in initial return of brain adenosine-triphosphate to normal after this "stress" followed by a progressive decline during the post-resuscitation period. In this study, substrate deficiency was investigated as a possible etiology for the decreased adenosine-triphosphate. Glucose and glucose-6-phosphate concentrations in the brain were measured before "stress" and after resuscitation and were found not to change, indicating no deficiency of substrate.
AuthorsH J Proctor, J J Wood
JournalSurgical neurology (Surg Neurol) Vol. 8 Issue 3 Pg. 225-6 (Sep 1977) ISSN: 0090-3019 [Print] United States
PMID897997 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)
Chemical References
  • Glucosephosphates
Topics
  • Animals
  • Brain (metabolism)
  • Disease Models, Animal
  • Glucosephosphates (metabolism)
  • Hypotension (metabolism)
  • Hypoxia (metabolism)
  • Male
  • Rats

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