Department of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, P. R. China.
Department of Anesthesia, Critical Care and Pain Medicine; Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129-2060, USA.
Sci Rep. 2020 Jul 8;10(1):11226. doi: 10.1038/s41598-020-66959-x.
Sevoflurane, a commonly used anesthetic, may cause agitation in patients. However, the mechanism underlying this clinical observation remains largely unknown. We thus assessed the effects of sevoflurane on neuronal activation and behaviors in mice. Ten-day-old mice received 2% sevoflurane, 1% isoflurane, or 6% desflurane for 10 minutes. The behavioral activities were recorded and evaluated at one minute after the loss of righting reflex in the mice, which was about two minutes after the anesthetic administration. The neuronal activation was evaluated by c-Fos expression and calcium imaging at one minute after the anesthetic administration. Propofol, which reduces neuronal activation, was used to determine the cause-and-effect of sevoflurane. We found that sevoflurane caused an increase in neuronal activation in primary somatosensory cortex of young mice and behavioral hyperactivity in the mice at one minute after the loss of righting reflex. Desflurane did not induce behavioral hyperactivity and isoflurane only caused behavioral hyperactivity with borderline significance. Finally, propofol attenuated the sevoflurane-induced increase in neuronal activation and behavioral hyperactivity in young mice. These results demonstrate an unexpected sevoflurane-induced increase in neuronal activation and behavioral hyperactivity in young mice. These findings suggest the potential mechanisms underlying the sevoflurane-induced agitation and will promote future studies to further determine whether anesthetics can induce behavioral hyperactivity via increasing neuronal activation.
七氟醚是一种常用的麻醉剂,可能会引起患者躁动。然而,这种临床观察的机制在很大程度上尚不清楚。因此,我们评估了七氟醚对小鼠神经元激活和行为的影响。10 日龄的小鼠接受 2%七氟醚、1%异氟醚或 6%地氟醚 10 分钟。在小鼠失去翻正反射后一分钟记录并评估行为活动,此时距麻醉给药后约 2 分钟。在麻醉给药后一分钟通过 c-Fos 表达和钙成像评估神经元激活。丙泊酚可减少神经元激活,用于确定七氟醚的因果关系。我们发现七氟醚在幼鼠初级体感皮层中引起神经元激活增加,并在失去翻正反射后一分钟引起小鼠行为过度活跃。地氟醚不会引起行为过度活跃,异氟醚仅引起行为过度活跃,但具有边缘显著性。最后,丙泊酚减轻了幼鼠中七氟醚引起的神经元激活增加和行为过度活跃。这些结果表明,七氟醚在幼鼠中引起了意外的神经元激活增加和行为过度活跃。这些发现提示了七氟醚引起躁动的潜在机制,并将促进未来的研究,以进一步确定麻醉剂是否可以通过增加神经元激活引起行为过度活跃。