Key result
Electric vagal nerve stimulation significantly reduced serum TNF-α levels compared to splenectomy alone (41.609 vs 61.028 pg/ml, P<0.001), though improvements in cognitive function were not statistically significant.
Why the study?
Inflammation caused by operation and general anesthesia contributes to early postoperation cognitive dysfunction, and the effects of electric vagal nerve stimulation on this dysfunction in aged rats were evaluated.
Does electric vagal nerve stimulation reduce inflammation and improve early postoperation cognitive dysfunction in aged rats?
Does electric vagal nerve stimulation reduce inflammation and improve early postoperation cognitive dysfunction in aged rats?
Electric vagal nerve stimulation reduces systemic and hippocampal inflammation following surgery in aged rats, though its effects on cognitive dysfunction are partial.
Supports anti-inflammatory effects of vagal stimulation in aged surgical models; leaves open cognitive benefits and clinical translation.
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 (SD) 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. qPCR was used to detected 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.
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Xiong et al. (2019) studied Postoperation cognitive dysfunction (n=33). Electric vagal nerve stimulation vs. Splenectomy without stimulation was evaluated on Serum TNF-α level (pg/ml) (p=<0.001). Electric vagal nerve stimulation significantly reduced serum TNF-α levels compared to splenectomy alone (41.609 vs 61.028 pg/ml, P<0.001), though improvements in cognitive function were not statistically significant.
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