Cerebral energy metabolite levels and survival following exposure to low inspired oxygen concentration.
To determine the relationship between brain energy metabolites and neurologic status after ischemia-hypoxia, we measured cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine, and lactate. Rats with permanent unilateral carotid occlusion were exposed to 5, 10, and 15 min of hypoxic atmosphere (FIO2 0.048) and, to examine metabolic restitution, 60 min after recovery in rats exposed to the same hypoxic mixture for 15 min. At 5 and 10 min of hypoxia, there were significant reductions in phosphocreatinine and elevations in tissue lactate, but only after 15 min of hypoxia, did ATP levels significantly decrease. By 60 min after recovery, phosphocreatinine values returned to the normal range, ATP values to 15% less than normal, and tissue lactate toward normal. In parallel survival studies, neurological status was examined following hypoxic exposure (PaO2 18 to 19 torr) for 5 an 10 min. Evidence for neurological injury in the form of posthypoxic seizures occurred at a point in time preceding significant changes in brain tissue ATP level. Since injury occurs prior to ATP reduction, changes in brain tissue ATP level may not be an appropirate endpoint for determining brain tissue injury in hypoxia.
D000255:Adenosine Triphosphate / Q000032:analysis*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D005260:Female; D000860:Hypoxia / Q000378:metabolism; D007773:Lactates / Q000032:analysis*; D008954:Models, Biological; D010100:Oxygen / Q000097:blood; D010725:Phosphocreatine / Q000032:analysis*; D051381:Rats
D007773:Lactates; D010725:Phosphocreatine; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate; D010100:Oxygen