Abstract
Elevations in prostaglandin E (PGE) have been documented in tumor and trauma patients. The physiologic significance of this elevation is not fully established. Utilizing a long-acting derivative of PGE, 16, 16-dimethyl-prostaglandin E (dPGE), in a rat model, we evaluated its effects on metabolic rates, amino acid, and neurotransmitter metabolism. dPGE was not found to significantly alter resting metabolic rate. It did decrease the plasma level of three amino acids, including tyrosine. Although dPGE also decreased brain tissue levels of tyrosine, no significant alterations were observed on amine neurotransmitters or metabolites.
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