Canadian Journal of Anesthesia, Vol 45, 860-864, Copyright © 1998 by Canadian Anesthesiologists' Society

ARTICLES

Cerebral oxygenation during prostaglandin E1 induced hypotension

Y Kadoi, S Saito, F Kunimoto, T Morita, F Goto, F Kawahara and N Fujita
Department of Anaesthesiology and Reanimatology, Gunma University, School of Medicine, Japan.

PURPOSE: To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E1 (PGE1) during fentanyl-oxygen anaesthesia. METHODS: Ten patients who underwent elective cardiac surgery received infusion of PGE1. After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO2) estimated by INVOS 3100R, PGE1 was continuously infused at 0.25-0.65 microgram.kg-1.min-1 (mean dosage: 410 +/- 41.4 mg.kg-1.min-1) 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 rSO2. Thirty minutes from the start of drug infusions, administration of PGE1 was stopped. The same parameters were measured again 10, 30 minutes after the stop of drug infusion. RESULTS: PGE1 decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE1 increased mixed venous saturation, but in contrast did not affect internal jugular pressure, internal jugular oxygen saturation and rSO2. CONCLUSIONS: These results suggest that PGE1 is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.

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