Cerebral oxygen and energy metabolism during and after 30 minutes of moderate hypoxia.
Sixty-four isolated canine brain preparations were subjected to either 15 or 30 min of perfusion with blood equilibrated at either Pao2 30 mmHg or Pao2 40 mmHg followed by up to 60 min of reoxygenation with blood having a Pao2 greater than 100 mmHg. Pao2 30 mmHg perfusion decreased oxygen availability and the cerebral metabolic rate for oxygen (CMRo2) to 44 and 49% of normal, respectively, whereas Pao2 40 mmHg perfusion decreased oxygen availability and CMRo2 to 64 and 70% of normal, respectively. Creatine phosphate was markedly decreased (0.6 and 4% of normal, respectively) and ATP was only slightly decreased (73 and 90% of normal, respectively) in these preparations during the hypoxic period. Although ATP returned to normal during the reoxygenation period in both groups, creatine phosphate and CMRo2 returned to normal only in the Pao2 40 mmHg preparations. In brains perfused at various Pao2 levels for periods ranging from 6 to 30 min, the total oxygen deficit (the cumulative difference over time between normal and actual CMRo2) rather than tissue lactate levels appeared to influence the restoration of CMRo2 to normal following hypoxia. An oxygen deficit in excess of 25 mumol/g precluded return to a normal CMRo2 following reoxygenation.(ABSTRACT TRUNCATED AT 250 WORDS)
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D004285:Dogs; D004569:Electroencephalography; D004734:Energy Metabolism; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D013997:Time Factors
D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate