Purpose: To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E t(PGEI) during fentanyl-oxygen anaesthesia. Methods: Ten patients who underwent elective cardiac surgery received infusion of PGE I . After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO2) estimated by INVOS 3100 R, PGE, was continuously infused at 0.25-0.65 ~g'kg -*'min -t (mean dosage: 410 -+ 41.4 mg'kg -* -min -*) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO 2. Thirty minutes from the start of drug infusions, administration of PGE, was stopped. The same parameters were measured again I 0, 30 minutes after the stop of drug infusion. Results: PGE, decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE, increased mixed venous saturation, but in contrast did not effect internal jugular pressure, internal jugular oxygen saturation and rSO 2. Conclusions: These results suggest that PGE, is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.Objectif : l~valuer les effets de l'hypotension, induite par la prostaglandine E,(PGE~), sur l'oxygEnation c&Ebrale pendant l'anesthEsie avec fentanyl et oxygEne. M&hodes : Dix patients qui devaient subir une chirurgie cardiaque Elective ont re~u une perfusion de PGE i. Apt& avoir procEdE ~ la gazomEtrie art&ielle de base, ~ celle du sang veineux mEIE et ~ celle de la veine jugulaire interne, EvaluE rhEmodynamie systEmique et la saturation en oxygEne cErEbral regional (SO2r) par INVOS 3100R, la PGE, a EtE administrEe en perfusion intraveineuse continue ~ 0,25-0,65/~g'kg -l'min -l (dosage moyen : 410 +_ 41,4 ~g.min-i). Dix, 20 et 30 minutes apr& le debut des perfusions de medicaments, les gaz du sang dEj~ cites ont &6 obtenus simultanEment avec la mesure de l'hEmodynamie systEmique et laSOzr. Trente minutes aprEs le debut des perfusions, l'administration de la PGE I a EtE arr&Ee. Les m~mes paramEtres ont EtE mesurEs encore aprEs I0 et 30 minutes apr~s rarr& de la perfusion de medicament. R~sultats : La PGE i abaisse la tension art&ielle moyenne (TAM) ~. 70 % de sa valeur de base environ (P < 0,05). La PGE, augmente la saturation en oxygEne du sang veineux m~IE mais, au contraire, n'a pas d'effet sur la tension de la veine jugulaire interne, sur la saturation en oxygEne de cette veine et sur la SO2r. Conclusion : Ces rEsultats montrent que la PGE, est un medicament appropriE pour induire de l'hypotension parce que le couplage dEbit/mEtabolisme du cerveau et l'oxygEnation cEr~brale rEgionale ont EtE maintenus pendant l'hypotension.