Sakarya University Faculty of Medicine Anesthesiology and Reanimation Department, Sakarya, Turkey.
Sakarya University Faculty of Medicine Pharmacology Department, Sakarya, Turkey.
Behav Brain Res. 2025 Feb 4;477:115290. doi: 10.1016/j.bbr.2024.115290. Epub 2024 Oct 11.
Postoperative cognitive dysfunction (POCD) encompasses a spectrum of cognitive impairments following surgery, attributed to disruptions in brain homeostasis. The pathogenesis involves glutamate toxicity, GABA receptor dysfunction, and alterations in NMDA and AMPA receptors. This study aimed to investigate the impact of pre-anesthetic amantadine administration on postoperative recovery time, POCD, and stress-related pain levels when combined with propofol anesthesia.
Twenty-four adult male BALB/C mice were divided into four groups: Control, Propofol, Amantadine, and Amantadine+Propofol. Amantadine and propofol doses were administered intraperitoneally based on previous literature. Recovery time, pain levels (assessed via tail pinch and hot plate tests), cognitive functions (evaluated through Morris Water Maze), and locomotor activity (measured via Open Field Test) were recorded.
Amantadine administration significantly reduced recovery time from propofol anesthesia, prolonged pain perception, and preserved cognitive functions compared to propofol alone. The time spent in the target quadrant in the Morris Water Maze was significantly longer in groups receiving amantadine. Additionally, the distance covered until finding the platform was significantly shorter in the propofol-only group.
Amantadine's neuroprotective effects, attributed to its antagonistic action on glutamate and NMDA receptors, mitigate the detrimental effects of propofol on cognitive function and pain perception. This study highlights the potential of combining amantadine with propofol to enhance postoperative outcomes.
Amantadine administration before propofol anesthesia positively influenced postoperative recovery, cognitive function preservation, and stress-related pain perception in mice. These findings suggest a potential therapeutic strategy to mitigate POCD and pain associated with surgery.
术后认知功能障碍（POCD）涵盖了手术后一系列认知障碍，归因于大脑内环境的破坏。发病机制涉及谷氨酸毒性、GABA 受体功能障碍以及 NMDA 和 AMPA 受体的改变。本研究旨在探讨麻醉前给予金刚烷胺对术后恢复时间、POCD 和与应激相关的疼痛水平的影响，同时结合丙泊酚麻醉。
将 24 只成年雄性 BALB/C 小鼠分为四组：对照组、丙泊酚组、金刚烷胺组和金刚烷胺+丙泊酚组。根据先前的文献，腹腔内给予金刚烷胺和丙泊酚。记录恢复时间、疼痛水平（通过尾巴捏和热板测试评估）、认知功能（通过 Morris 水迷宫评估）和运动活动（通过旷场试验测量）。
与单独使用丙泊酚相比，金刚烷胺给药显著缩短了丙泊酚麻醉后的恢复时间，延长了疼痛感知时间，保留了认知功能。在接受金刚烷胺的组中，在 Morris 水迷宫中停留在目标象限的时间明显更长。此外，在仅使用丙泊酚的组中，找到平台的距离明显缩短。
金刚烷胺的神经保护作用归因于其对谷氨酸和 NMDA 受体的拮抗作用，减轻了丙泊酚对认知功能和疼痛感知的不利影响。本研究强调了在丙泊酚麻醉前联合使用金刚烷胺以改善术后结果的潜力。
在丙泊酚麻醉前给予金刚烷胺对小鼠术后恢复、认知功能保存和应激相关疼痛感知产生积极影响。这些发现提示了一种潜在的治疗策略，可以减轻与手术相关的 POCD 和疼痛。
