1. The current experiments studied the effects of the inhalation anesthetic, isoflurane, on 5-hydroxytryptamine (5-HT) metabolism, protein synthesis, and angiotensin-converting enzyme activity in perfused rat lungs. 2. Under first order reaction conditions, isoflurane decreased the accumulation of tissue 5-hydroxyindoleacetic acid, the principle metabolite of 5-HT in a concentration-related, competitive, and reversible manner, indicating inhibition of endothelial 5-HT uptake. 3. In apparent contrast, isoflurane appeared to stimulate uptake of 5-HT by an imipramine-sensitive process, into a cell type unable to metabolize the parent amine. 4. Isoflurane increased absolute angiotensin-converting enzyme activity only at an inspired concentration of 5%. The anesthetic did not affect lung protein synthesis.
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