Abstract

Application of commonly used volatile anesthetics after brain ischemia onset (post-treatment) provides neuroprotection in rodents. To further test its translational potential, this study was designed to determine whether isoflurane post-treatment induced neuroprotection in rabbits after embolic stroke. White male New Zealand rabbits received intra-carotid injection of clots when they were awake. Some rabbits were exposed to 2.5% isoflurane for 1 h at 5 min after the injection. Isoflurane post-treatment increased the tolerance of rabbits to the amount of clots. Isoflurane post-treatment also reduced brain infarct volumes and plasma S100B 3 days after the injection of 5 mg clots and improved neurological deficit scores after the stroke. Isoflurane post-treatment improves neurological outcome in rabbits after embolic stroke.

Highlights

  • Volatile anesthetics are the most commonly used general anesthetics in human in the U.S.A

  • Our results clearly suggest that isoflurane post-treatment provides neuroprotection in rabbits after an embolic stroke

  • A highly clinical relevant stroke model was used to test this neuroprotection. These results suggest the translational potential of isoflurane post-treatment in human; especially in the context that isoflurane has been used safely in clinical practice for decades

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Summary

Introduction

Volatile anesthetics are the most commonly used general anesthetics in human in the U.S.A. Application of the currently clinically used volatile anesthetics, such as isoflurane and sevoflurane, after the onset of brain ischemia (post-treatment or post-conditioning) reduces ischemic brain injury [1,2,3]. Application of the currently clinically used volatile anesthetics, such as isoflurane and sevoflurane, after the onset of brain ischemia (post-treatment or post-conditioning) reduces ischemic brain injury [1,2,3] These effects have been shown in rodents whose brain ischemia is induced by intravascular suture technique. We designed this study to determine whether isoflurane post-treatment induced neuroprotection in rabbits after an embolic stroke that is the model used to establish the effectiveness of tissue plasminogen activator therapy [5]

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