• Beatrice Beck-Schimmer, Tanja Restin, Carl Muroi, Roth Z'GraggenBirgitB, Emanuela Keller, and Martin Schläpfer.
• From the Institute of Physiology and Zurich Centre for Integrative Human Physiology, University of Zurich (BBS, TR, BRZ, MS), Institute of Anaesthesiology, University Hospital Zurich, Zurich, Switzerland (BBS, TR, MS), Department of Anesthesiology, University of Illinois at Chicago, Chicago, USA (BBS) and Neurosurgical Intensive Care Unit, University Hospital Zurich, Zurich, Switzerland (CM, EK).
• Eur J Anaesthesiol. 2020 May 1; 37 (5): 402412402-412.

BackgroundSevere neurological impairment is a problem after subarachnoid haemorrhage (SAH). Although volatile anaesthetics, such as sevoflurane, have demonstrated protective properties in many organs, their use in cerebral injury is controversial. Cerebral vasodilation may lead to increased intracranial pressure (ICP), but at the same time volatile anaesthetics are known to stabilise the SAH-injured endothelial barrier.ObjectiveTo test the effect of sevoflurane on ICP and blood-brain barrier function.DesignRandomised study.ParticipantsOne hundred male Wistar rats included, 96 analysed.InterventionsSAH was induced by the endoluminal filament method under ketamine/xylazine anaesthesia. Fifteen minutes after sham surgery or induction of SAH, adult male Wistar rats were randomised to 4 h sedation with either propofol or sevoflurane.Main Outcome MeasuresMean arterial pressure (MAP), ICP, extravasation of water (small), Evan's blue (intermediate) and IgG (large molecule) were measured. Zonula occludens-1 (ZO-1) and beta-catenin (β-catenin), as important representatives of tight and adherens junction proteins, were determined by western blot.ResultsPropofol and sevoflurane sedation did not affect MAP or ICP in SAH animals. Extravasation of small molecules was higher in SAH-propofol compared with SAH-sevoflurane animals (79.1 ± 0.9 vs. 78.0 ± 0.7%, P = 0.04). For intermediate and large molecules, no difference was detected (P = 0.6 and P = 0.2). Both membrane and cytosolic fractions of ZO-1 as well as membrane β-catenin remained unaffected by the injury and type of sedation. Decreased cytosolic fraction of β-catenin in propofol-SAH animals (59 ± 15%) was found to reach values of sham animals (100%) in the presence of sevoflurane in SAH animals (89 ± 21%; P = 0.04).ConclusionThis experiment demonstrates that low-dose short-term sevoflurane sedation after SAH in vivo did not affect ICP and MAP and at the same time may attenuate early brain oedema formation, potentially by preserving adherens junctions.Trial RegistrationNo 115/2014 Veterinäramt Zürich.

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