Cerebral monoamine and energy metabolism during recovery from hypoxia-oligemia.
The effects of 30 min of exposure to arterial Po2's of 25-27 mmHg and right carotid artery occlusion upon the cerebral monoamine and energy metabolism were studied in lightly anesthetized rats following reoxygenation for 0, 30, and 60 min. At 0 min of recovery the clamped hemisphere showed decreases in ATP and increases in ADP, AMP, and lactate which indicated an advanced disturbance of the tissues' mitochondrial function. At 0 min of recovery the tryptophan hydroxylation rate was 40% of control, whereas tyrosine hydroxylation was unchanged. Removal of the clamp and reoxygenation for 60 min resulted in a normalization of oxidative metabolism and aromatic amino acid hydroxylase function and thus indicated no permanent detectable defect of these processes in the restituted hypoxemic-oligemic brain.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001810:Blood Volume; D001921:Brain / Q000378:metabolism*; D050260:Carbohydrate Metabolism; D004734:Energy Metabolism; D006900:Hydroxylation; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D051381:Rats / Q000378:metabolism; D013997:Time Factors; D014364:Tryptophan / Q000378:metabolism*; D014443:Tyrosine / Q000378:metabolism*
D000227:Adenine Nucleotides; D014443:Tyrosine; D014364:Tryptophan