Brain metabolism after 30 minutes of hypoxic or anoxic perfusion or ischemia.
In 48 separate experiments, isolated canine brain preparations were subjected to 30 min of either hypoxic (PaO2 congruent to 20 mmHg) perfusion, anoxic (PaO2 < 10 mmHg) perfusion, or total ischemia followed by reperfusion for up to 2 h with normal oxygenated blood. Unlike ischemia and anoxia, energy metabolism was sufficient during hypoxia to maintain substantial levels of ATP (48% of normal), sustain normal ion gradients, and prevent edema formation. Posthypoxia metabolism was adequate to clear accumulated lactate, enable recovery of normal tissue glucose levels, and allow return to normal levels of glycolytic intermediates. Although not as complete as that following hypoxia, recovery from cerebral edema and restoration of metabolism were better in ischemic than anoxic cortex. The reduced oxygen uptake in all groups during reoxygenation (55% of normal) indicates that all have a diminished capacity for energy metabolism. The ATP levels recovered more rapidly after 15 min of reoxygenation in the anoxic (57% of normal) than in the ischemic (21% of normal) group. Thus ATP does not appear to be directly related to recovery from edema.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001929:Brain Edema / Q000378:metabolism; D004285:Dogs; D004569:Electroencephalography; D004573:Electrolytes / Q000378:metabolism; D006019:Glycolysis; D002534:Hypoxia, Brain / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D051381:Rats; D014655:Vascular Resistance
D001786:Blood Glucose; D004573:Electrolytes; D000255:Adenosine Triphosphate; D010100:Oxygen