Department of Anesthesia, Tianjin Medical University General Hospital, Tianjin, China (mainland).
Tianjin Institute of Anesthesiology, Tianjin, China (mainland).
Med Sci Monit. 2021 Sep 26;27:e932422. doi: 10.12659/MSM.932422.
BACKGROUND Perioperative neuro-cognitive disorders (PND) are preoperative and postoperative complications of multiple nervous systems, typically manifested as decreased memory and learning ability after surgery. It was used to replace the original definition of postoperative cognitive dysfunctions (POCD) from 2018. Our previous studies have shown that sevoflurane inhalation can lead to cognitive dysfunction in Sprague-Dawley rats, but the specific mechanism is still unclear. MATERIAL AND METHODS Thirty-six male Sprague-Dawley rats were randomly divided into 6 groups (n=6): the SD group was given 24-h acute sleep deprivation; Sevoflurane was inhaled for 2 h in the Sevo group. Two mL propofol was injected into the tail vein of rats in the Prop group. The rats in the SD+Sevo group and SD+Prop group were deprived of sleep before intervention in the same way as before. RESULTS We noted significant behavioral changes in rats treated with SIK3 inhibitors or tau phosphorylation agonists before propofol injection or sevoflurane inhalation, with associated protein levels and dendritic spine density documented. Sevoflurane anesthesia-induced cognitive impairment following acute sleep deprivation was more pronounced than sleep deprivation-induced cognitive impairment alone and resulted in increased brain SIK3 levels, increased phosphorylation of total tau and tau, and decreased acetylation modifications. After using propofol, the cognitive function returned to baseline levels with a series of reversals of cognitive dysfunction. CONCLUSIONS These results suggest that sevoflurane inhalation via the SIK3 pathway aggravates cognitive impairment after acute sleep deprivation and that propofol anesthesia reverses the effects of sleep deprivation by affecting modifications of tau protein.
围手术期神经认知障碍（PND）是多种神经系统的术前和术后并发症，通常表现为手术后记忆力和学习能力下降。它于 2018 年被用来替代术后认知功能障碍（POCD）的原始定义。我们之前的研究表明，七氟醚吸入可导致 Sprague-Dawley 大鼠认知功能障碍，但具体机制尚不清楚。
36 只雄性 Sprague-Dawley 大鼠随机分为 6 组（n=6）：SD 组给予 24 小时急性睡眠剥夺；Sevo 组吸入七氟醚 2 小时。在 Prop 组中，将 2 mL 丙泊酚注入大鼠尾静脉。SD+Sevo 组和 SD+Prop 组在干预前以与之前相同的方式剥夺睡眠。
在丙泊酚注射或七氟醚吸入之前，我们注意到使用 SIK3 抑制剂或 tau 磷酸化激动剂治疗的大鼠出现明显的行为变化，并记录了相关的蛋白水平和树突棘密度。急性睡眠剥夺后七氟醚麻醉引起的认知障碍比单独睡眠剥夺引起的认知障碍更为明显，导致大脑 SIK3 水平升高，总 tau 和 tau 磷酸化增加，乙酰化修饰减少。使用丙泊酚后，认知功能恢复基线水平，一系列认知功能障碍得到逆转。
这些结果表明，七氟醚通过 SIK3 途径吸入会加重急性睡眠剥夺后认知障碍，丙泊酚麻醉通过影响 tau 蛋白的修饰来逆转睡眠剥夺的影响。
