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BJA Advance Access originally published online on September 6, 2006
British Journal of Anaesthesia 2006 97(5):617-623; doi:10.1093/bja/ael238
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

ß2 Adrenergic antagonist inhibits cerebral cortical oxygen delivery after severe haemodilution in rats

G. M. T. Hare1,2,*, J. M. A. Worrall1, A. J. Baker1, E. Liu1, N. Sikich1 and C. D. Mazer1,2

1 Department of Anaesthesia and the Cara Phelan Centre for Trauma Research, University of Toronto, St Michael's Hospital 30 Bond Street, Toronto, Ontario M5B 1W8, Canada
2 Department of Physiology, University of Toronto 1 King's College Circle, Toronto, Ontario, M5S 1A8, Canada

*Corresponding author: Department of Anaesthesia and Physiology, University of Toronto, St Michael's Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada. E-mail: hareg{at}smh.toronto.on.ca

Background. Haemodilution has been associated with neurological morbidity in surgical patients. This study tests the hypothesis that inhibition of cerebral vasodilatation by systemic ß2 adrenergic blockade would impair cerebral oxygen delivery leading to tissue hypoxia in severely haemodiluted rats.

Methods. Under general anaesthesia, cerebral tissue probes were placed to measure temperature, regional cerebral blood flow (rCBF) and tissue oxygen tension (PBrO2) in the parietal cerebral cortex or hippocampus. Baseline measurements were established before and after systemic administration of either a ß2 antagonist (10 mg kg–1 i.v., ICI 118, 551) or saline vehicle. Acute haemodilution was then performed by simultaneously exchanging 50% of the estimated blood volume (30 ml kg–1) with pentastarch. Arterial blood gases (ABGs), haemoglobin concentration (co-oximetry), mean arterial blood pressure (MAP) and heart rate (HR) were also measured. Data were analysed using a two-way ANOVA and post hoc Tukey's test [mean (SD)].

Results. Haemodilution reduced the haemoglobin concentration comparably in all groups [71 (9) g litre–1]. There were no differences in ABGs, co-oximetry, HR and MAP measurements between control and ß2 blocked rats, either before or 60 min after drug or vehicle administration. In rats treated with the ß2 antagonist there was a significant reduction in parietal cerebral cortical temperature, regional blood flow and tissue oxygen tension, relative to control rats, 60 min after haemodilution (P<0.05 for each). These differences were not observed when probes were placed in the hippocampus.

Conclusion. Systemic ß2 adrenergic blockade inhibited the compensatory increase in parietal cerebral cortical oxygen delivery after haemodilution thereby reducing cerebral cortical tissue oxygen tension.


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