Key result
Electric vagal nerve stimulation significantly reduced surgery-induced systemic inflammation, lowering serum TNF-α levels compared to control (41.609 vs 61.028 pg/ml, p<0.001), though improvements in postoperative cognitive dysfunction were not statistically significant.
Why the study?
Does electric vagal nerve stimulation improve postoperation cognitive dysfunction and reduce inflammation in aged rats?
Does electric vagal nerve stimulation improve postoperation cognitive dysfunction and reduce inflammation in aged rats?
Electric vagal nerve stimulation reduces surgery-induced inflammation in aged rats, though its protective effects on cognitive dysfunction require further optimization.
Vagal stimulation curbs postoperative inflammation in aged rats; leaves open whether optimized protocols can protect cognition before human trials.
Objective This study aimed to evaluate effects of vagal nerve stimulation on postoperation cognitive dysfunction in aged rats. Material and Methods: A total of 33 male SD rats were ssigned randomly to three groups, the control group, the s group and sv group. Behavior and memory were evaluated by Open Field Test and Morris Water Maze. The cytokines level were measured by ELISA. The TNF-α protein in hippocampal zone were assessed by Western blotting. qPCR was used to detected the mRNA expression of NF-κB in hippocampus. Results: During the anesthesia/operation, the vital life signs of rats were stable. In SV group, vagal nerve stimulation could decrease heart rate lower than 10% of basic level and kept it at a stable range by regulation of stimulation intensity. After stimulation stop, the heart rate would return to the basic level again. This indicated that the model of vagal nerve stimulation was successful. The serum inflammatory cytokines of TNF-α and IL-6 increased by the operation/anesthesia, but these cytokines could be decreased by the vagal nerve stimulation (all P<0.05). The level of TNF-α protein and mRNA expression of NF-κB in hippocampus were also eliminated by the vagal nerve stimulation compared to S group (P<0.05). The Morris Water Maze results showed the escape latency of postoperation in the S group was significantly longer than the C group (P<0.05), and the times of crossing platform in the S group was lower than that of the C group (P<0.05). Although the escape latency of postopration in the SV group was shorter than that of the S group, there was no significant difference between two groups. There were no significant differences in behavior test by Open Field test between three groups. Conclusion The inflammation caused by the operation and general anesthesia was an important reason of postoperation cognitive dysfunction, and electric vagal nerve stimulation could inhibit this inflammation. Meanwhile, vagal nerve stimulation could ameliorate postoperation cognitive dysfunction partly, but the protective effects were not enough and should be studied and improved in the future.
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Xiong et al. (2019) studied Postoperation cognitive dysfunction (n=33). Electric vagal nerve stimulation vs. Splenectomy and general anesthesia without vagal nerve stimulation was evaluated on Serum TNF-α level (pg/ml) (p=<0.001). Electric vagal nerve stimulation significantly reduced surgery-induced systemic inflammation, lowering serum TNF-α levels compared to control (41.609 vs 61.028 pg/ml, p<0.001), though improvements in postoperative cognitive dysfunction were not statistically significant.
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