Serotonin is a vasoconstrictor thought to cause coronary artery constriction in humans. The purpose of this study was to determine if isoflurane and halothane each attenuate coronary artery constriction evoked by serotonin in pigs. Bothin vitroandin vivoexperimental methods were used. Isolated coronary arteries with and without endothelium were studied in organ chambers in the presence and absence of 2.5% concentrations of the anesthetics. In intact pigs serotonin was infused directly into the left anterior descending coronary arteries to induce constriction. The vasodilator effects of 0.5%, 1.25%, and 2.0% isoflurane and halothane were determined using quantitative angiography. Contractile responses of isolated coronary arteries were depressed by the two anesthetics. Maximum contractile responses to serotonin were as follows: rings with endothelium 45 ± 5% untreatedversus29 ± 5% with isoflurane 2.5% (difference between dose-response curves,P< 0.01) and without endothelium 67 ± 5% untreatedversus51 ± 6% with isoflurane 2.5% (P< 0.001); with endothelium 52 ± 7% untreatedversus28 ± 7% with halothane 2.5% (P< 0.001) and without endothelium 65 ± 5% untreatedversus40 ± 6% with halothane 2.5% (P< 0.001). In intact pigs isoflurane and halothane dilated constricted coronary arteries with and without endothelium at all anesthetic concentrations tested, including concentrations as low as 0.5%. Isoflurane 1.25% increased diameter of vessels with endothelium from 1.5 ± 0.1 mm to 1.7 ± 0.1 mm (P< 0.02) and halothane 1.25% increased diameter from 1.6 ± 0.1 mm to 1.7 ± 0.1 mm (P< 0.01). In vessels without endothelium isoflurane 1.25% increased diameter from 1.8 ± 0.1 mm to 2.0 ± 0.1 mm (P< 0.01) and halothane 1.25% increased diameter from 1.9 ± 0.1 mm to 2.0 ± 0.2 mm (P< 0.01). Results demonstrate that isoflurane and halothane attenuate contractile responses evoked by serotonin in pig coronary arteries studied bothin vitroandin vivo.