Abstract
It is hypothesized that central nervous system inflammation induced by systematic inflammation due to surgical trauma plays a critical role in postoperative cognitive dysfunction. The potential inhibitory effect of nerve blockage with local anesthetics on peripheral inflammatory response has been reported. We hypothesize that nerve blockage may be effective in reducing postoperative inflammation and cognitive decline. The rats at the age of 4 weeks were subjected to general anesthesia and humeral fracture fixation, in combination with brachial plexus block, saline versus ropivacaine, respectively. The rats from control group underwent general anesthesia only. The expression of proinflammatory cytokines in plasma and in hippocampus was measured. Open field test and new object recognition task were performed before surgery and on postoperative days (POD) 1, 3, and 7. Compared with control group, the level of cytokines in plasma and hippocampus revealed an obvious increase in surgery groups. The effect of brachial plexus block on decreasing cytokines was observed. The rats exposed to surgery without brachial plexus block showed behavior impairment. Our results indicated that nerve blockage could downregulate proinflammatory cytokines in hippocampus after humeral fixation surgery, which may ameliorate the postoperative cognitive dysfunction in young rats.
Highlights
Accumulated evidence indicated that surgery-induced central nervous system (CNS) inflammation plays a key role in postoperative-deteriorated cognitive function [1,2,3,4,5,6,7]
In order to explore whether surgical injury and nerve blockage therapy can alter inflammatory cytokines in blood, plasma level of IL-1β, IL-6, and tumor necrosis factor-α (TNF-α) was measured
Young rats from fracture group without performing brachial plexus block revealed an upregulated release of plasma/hippocampal proinflammatory cytokines and suffered postoperative cognitive impairment
Summary
Accumulated evidence indicated that surgery-induced central nervous system (CNS) inflammation plays a key role in postoperative-deteriorated cognitive function [1,2,3,4,5,6,7]. Inflammatory response of CNS is a part of systemic inflammation. Surgical trauma can initiate peripheral immune activation, thereby leading to systemic cascade responses of proinflammatory cytokines [8,9,10]. The peripherally originating proinflammatory cytokines may enter into CNS through a direct or indirect way [9, 11]. Excessive inflammatory mediators in brain can influence postoperative learning development. If the responses triggered by surgical noxious stimuli were inhibited, CNS inflammation may be attenuated and postoperative cognitive dysfunction can be mitigated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
