Effects of promethazine on the energy metabolism of normoxic and hypoxic rat brain.
The metabolic effects of intraperitoneal administration of promethazine on normoxic, hypoxemic and hypoxemic-oligemic rat brain were assessed by measurement of the cerebral contents of energy phosphates, and selected glycolytic-citric acid cycle intermediates. In normoxic brain promethazine (25-100 mg/kg-1) was associated with unaltered adenylates, increased glucose and aspartate and decreased pyruvate, lactate and malate; a pattern which was compatible with cerebral metabolic depression. Hypoxemic animals receiving either saline or promethazine (25 mg/kg-1) showed equivalent decreases in ATP and increases in lactate which indicated that promethazine had no significant effect on the metabolism of the acutely hypoxic brain. In animals exposed to hypoxemia plus right carotid artery occlusion (oligemia) the promethazine treated group (25 mg/kg-1) showed significantly lower ATP and higher AMP contents which suggested an adverse effect on the metabolism of the acutely hypoxic-oligemic brain. It is concluded that promethazine does not beneficially alter the energy metabolism of the acutely hypoxic or hypoxic-oligemic brain.
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects*; D002534:Hypoxia, Brain / Q000188:drug therapy / Q000378:metabolism*; D008297:Male; D008954:Models, Biological; D010101:Oxygen Consumption / Q000187:drug effects; D011398:Promethazine / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D011919:Rats, Inbred Strains
D000227:Adenine Nucleotides; D011398:Promethazine