• A Holmström, I Rosén, and J Akeson.
• Department ofAnaesthesia and Intensive Care, Malmö University Hospital, Lund University, Malmö, Sweden. anders.holmstrom@skane.se
• Acta Anaesthesiol Scand. 2004 Apr 1;48(4):400-4.

BackgroundIn clinical neuroanaesthesia, the increase in cerebral blood flow (CBF) and intracranial pressure caused by the cerebral vasodilative effects of an inhalational anaesthetic agent is counteracted by the cerebral vasoconstriction induced by hypocapnia. Desflurane and sevoflurane may have advantages over the more traditionally used isoflurane in neuroanaesthesia but their dose-dependent vasodilative effects at hypocapnia have not been compared in the same model using truly equipotent minimal alveolar concentrations (MACs).MethodDesflurane, sevoflurane and isoflurane were administered in a randomized order to six pigs at 0.5 and 1.0 MAC. The intra-arterial xenon clearance technique was used to calculate CBF. Blood pressure was invasively monitored. Cerebral and systemic physiological variables were recorded first at normocapnia (PaCO2 5.6 kPa) and then at hypocapnia (PaCO2 3.5 kPa). Electroencephalographic (EEG) activity was continuously recorded.ResultsNone of the three agents abolished cerebrovascular reactivity to hyperventilation, and at 0.5 MAC all had similar effects on CBF at hypocapnia. Desflurane at 1.0 MAC was associated with 16% higher CBF (P = 0.027) at hypocapnia than isoflurane, and with 24% higher CBF (P = 0.020) than sevoflurane. There was no seizure activity in the EEG.ConclusionMore cerebral vasodilation at hypocapnia with high doses of desflurane than with sevoflurane or isoflurane indicates that desflurane might be less suitable for neuroanaesthesia than sevoflurane and isoflurane.

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