Role of glucose-6-phosphate in cerebral dysfunction following hypoxia and hypotension.
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.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D004195:Disease Models, Animal; D005958:Glucosephosphates / Q000378:metabolism*; D007022:Hypotension / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D051381:Rats
D005958:Glucosephosphates