Jun Xiong1, Huijun Wang2, Yin Bao2, Yuliang Guo2, Yongxing Sun3. 1. Department of Anesthesiology, Sanbo Brain Hospital, Capital Medical University, No. 50 Yikesong, Xiangshan, Haidian District, Beijing, 100093, China. 2. Department of Anesthesiology, Tongren Hospital, Capital Medical University, No. 1 Dongjiao Minxiang, Dongcheng District, Beijing, 100730, China. 3. Department of Anesthesiology, Sanbo Brain Hospital, Capital Medical University, No. 50 Yikesong, Xiangshan, Haidian District, Beijing, 100093, China. B2008194@126.com.
Abstract
BACKGROUND: This study aimed to evaluate effects of electric vagal nerve stimulation on early postoperation cognitive dysfunction in aged rats. METHODS: A total of 33 male Sprague Dawley rats were selected and assigned randomly to three groups, control group (C, n = 10), splenectomy group (S, n = 10) and splenectomy+vagal nerve stimulation group (SV, n = 13). Behavior and memory of rats were evaluated by Open Field Test and Morris Water Maze. Levels of TNF-α, IL-6 and IL-10 in serum were measured by ELISA. The level of TNF-α protein in hippocampus was assessed by Western blotting. rt-PCR was used to detect mRNA expression of NF-κB in hippocampus. RESULTS: During anesthesia/operation, vital life signs of rats were stable. In SV group, vagal nerve stimulation decreased heart rate lower than 10% of basic level and kept it at a stable range by regulating stimulation intensity. After stimulation stop, heart rate returned to the basic level again. This indicated that the model of vagal nerve stimulation was successful. Serum levels of TNF-α and IL-6 increased by the operation/anesthesia, but they decreased with vagal nerve stimulation (all P < 0.05). TNF-α protein and mRNA expression of NF-κB in hippocampus were also eliminated by vagal nerve stimulation compared to S group (P < 0.05). Results of Morris Water Maze showed escape latency of postoperation in S group was significantly longer than C group (P < 0.05), and times of crossing platform in S group was lower than that of C group (P < 0.05). Although escape latency of postopration in SV group was shorter than that of S group, there was no significant difference between two groups. Meanwhile there were no significant differences of behavior test in Open Field test between three groups, although vagal nerve stimulation improved partly active explore behavior compared to S group. CONCLUSION: The inflammation caused by operation and general anesthesia was an important reason of early postoperation cognitive dysfunction, and electric vagal nerve stimulation could inhibit the inflammation. Meanwhile, vagal nerve stimulation could ameliorate early postoperation cognitive dysfunction partly, but its protective effects were not enough and should be studied and improved in future.
BACKGROUND: This study aimed to evaluate effects of electric vagal nerve stimulation on early postoperation cognitive dysfunction in aged rats. METHODS: A total of 33 male Sprague Dawley rats were selected and assigned randomly to three groups, control group (C, n = 10), splenectomy group (S, n = 10) and splenectomy+vagal nerve stimulation group (SV, n = 13). Behavior and memory of rats were evaluated by Open Field Test and Morris Water Maze. Levels of TNF-α, IL-6 and IL-10 in serum were measured by ELISA. The level of TNF-α protein in hippocampus was assessed by Western blotting. rt-PCR was used to detect mRNA expression of NF-κB in hippocampus. RESULTS: During anesthesia/operation, vital life signs of rats were stable. In SV group, vagal nerve stimulation decreased heart rate lower than 10% of basic level and kept it at a stable range by regulating stimulation intensity. After stimulation stop, heart rate returned to the basic level again. This indicated that the model of vagal nerve stimulation was successful. Serum levels of TNF-α and IL-6 increased by the operation/anesthesia, but they decreased with vagal nerve stimulation (all P < 0.05). TNF-α protein and mRNA expression of NF-κB in hippocampus were also eliminated by vagal nerve stimulation compared to S group (P < 0.05). Results of Morris Water Maze showed escape latency of postoperation in S group was significantly longer than C group (P < 0.05), and times of crossing platform in S group was lower than that of C group (P < 0.05). Although escape latency of postopration in SV group was shorter than that of S group, there was no significant difference between two groups. Meanwhile there were no significant differences of behavior test in Open Field test between three groups, although vagal nerve stimulation improved partly active explore behavior compared to S group. CONCLUSION: The inflammation caused by operation and general anesthesia was an important reason of early postoperation cognitive dysfunction, and electric vagal nerve stimulation could inhibit the inflammation. Meanwhile, vagal nerve stimulation could ameliorate early postoperation cognitive dysfunction partly, but its protective effects were not enough and should be studied and improved in future.
Entities:
Keywords:
Cognitive dysfunction; General anesthesia; Inflammation; Vagus nerve stimulation
Authors: William J Huffman; Saraswathi Subramaniyan; Ramona M Rodriguiz; William C Wetsel; Warren M Grill; Niccolò Terrando Journal: Brain Stimul Date: 2018-10-09 Impact factor: 8.955