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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.
REPORTS OF INVESTIGATION 767CAN J ANESTH 2000 / 47: 8 / pp [767][768][769][770][771][772][773][774] Purpose: Several different anti-hypertensive regimens have been introduced for the prevention of systemic hyperdynamic responses after electrically induced seizures. In the present study, the effects of anti-hypertensive medications on cerebral circulation were studied.Methods: Systemic blood pressure was controlled by several anti-hypertensive medications, nicardipine, prostaglandin E1, alprenolol and nitroglycerin, in 30 patients (150 electroconvulsive therapy trials). Changes in cerebral blood flow velocity were measured by transcranial Doppler sonography of the right middle cerebral artery from the start of anesthesia to 10 min after the electrical shock.Results: Administration of a Ca 2+ antagonist, nicardipine, or prostaglandin E1 did not alter the augmented cerebral blood flow velocity after the seizure. However, a ß-adrenergic blocking agent, alprenolol (P < 0.05) or nitroglycerin (P < 0.01) partially inhibited the increase in cerebral blood flow velocity. Maximal blood flow velocity was 133% larger than the pre-anesthesia value in the control group, 109% in the nicardipine group, 113% in the prostaglandin E1 group, 72% in the alprenolol group, and 45% in the nitroglycerin group, respectively. The increase in cerebral blood flow velocity after electrically induced seizure was independent of systemic blood pressure. Internal jugular venous saturation (SjO 2 ) was increased, and difference in arterial and venous concentrations of lactate was not altered in all groups.Conclusions: Cerebral hemodynamics is altered by ECT, even when systemic hemodynamics are stabilized by antihypertensive medication. Although the effects of antihypertensive medicine on cerebral hemodynamics are variable, systemic blood pressure control by these agents does not induce cerebral ischemia after ECT.Objectif : Différentes thérapies antihypertensives ont été proposées comme moyen de prévention des répon-ses hyperdynamiques généralisées à la suite d'électrochocs. Dans la présente étude, on a analysé les effets de médicaments antihypertenseurs sur la circulation cérébrale.Méthode : La pression sanguine générale a été contrôlée par différents médicaments antihypertenseurs, la nicardipine, la prostaglandine E 1 , l'alprénolol et la nitroglycérine, chez 30 patients lors de 150 essais d'électro-chocs. Les changements de vitesse circulatoire cérébrale ont été mesurés par échographie Doppler transcrâni-enne de l'artère cérébrale moyenne droite, du début de l'anesthésie jusqu'à 10 min après l'électrochoc.Résultats : L'administration d'un antagoniste de Ca 2 +, la nicardipine, ou la prostaglandine E 1 n'ont pas modifié la vitesse circulatoire cérébrale augmentée après les convulsions. Toutefois, un agent ß-bloquant, l'alprénolol (P < 0,05) ou la nitroglycérine (P < 0,01) ont partiellement inhibé l'augmentation de vitesse circulatoire cérébrale. La vitesse circulatoire maximale a été 133 % de la valeur préanesthésique mesurée dans le groupe tém...
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