OBJECTIVE: This study aimed to investigate the effects of dexmedetomidine on cerebral oxygen saturation [Sct(O 2 )] and postoperative cognitive function in elderly patients undergoing minimally invasive coronary artery bypass graft surgery. METHODS: Sixty elderly patients who received minimally invasive coronary artery bypass graft surgery were randomly equally divided into dexmedetomidine group (group D) and control group (group N). The patients in group D were pumped with 1 g/kg dexmedetomidine for 15 min before incision, followed by continuous pumping at 0.3-0.5 g/(kg•h) till the end of the operation. The patients in group N received same dose of normal saline during the operation. Sct(O 2 ) was monitored at pre-induction (T0), post-induction (T1), 30 min (T2) after single-lung ventilation, and after surgery (T3). Mini-mental state examination (MMSE) was used to assess the cognitive function at 1 day before, 72 hour and 7 days after surgery. RESULTS: Sct(O 2 ) level in group D was significantly higher than that in group N at T2 (P < 0.05). Sct(O 2 ) level was statistically lower at T2 than that at T0, T1 and T3 in the same group N (P < 0.05). At 72 h and 7d after operation, the incidence of cognitive dysfunction in group D was markedly lower than that in group N (P < 0.05), the MMSE score in group D was markedly higher than those in group N, but was significantly lower than that before surgery (P < 0.05). CONCLUSION: Dexmedetomidine can alleviate the decrease of Sct(O 2 ) during single-lung ventilation, improve postoperative cognitive function, and reduce the incidence of POCD in elderly patients with minimally invasive coronary artery bypass surgery.
Background:This meta-analysis aimed to assess the efficiency and safety of intravenous infusion of lidocaine for pain management after laparoscopic cholecystectomy (LC).Methods:A systematic search was performed in PubMed (August 1966–2017), Medline (August 1966–2017), Embase (August 1980–2017), ScienceDirect (August 1985–2017), and the Cochrane Library. Only randomized controlled trials (RCTs) were included. Fixed/random effect model was used according to the heterogeneity tested by I2 statistic. Meta-analysis was performed using Stata.11.0 software.Results:A total of 5 RCTs were retrieved involving 274 patients. The present meta-analysis indicated that there were significant differences between groups in terms of visual analog scale scores at 12hours (weighted mean difference [WMD]=−0.743, 95% CI: −1.246 to −0.240, P = .004), 24hours (WMD=−0.712, 95% CI: −1.239 to −0.184, P = .008), and 48hours (WMD=−0.600, 95% CI: −0.972 to −0.229, P = .002) after LC. Significant differences were found regarding opioid consumption at 12hours (WMD=−3.136, 95% CI: −5.591 to −0.680, P = .012), 24hours (WMD=−4.739, 95% CI: −8.291 to −1.188, P = .009), and 48hours (WMD=−3.408, 95% CI: −5.489 to −1.326, P = .001) after LC.Conclusion:Intravenous lidocaine infusion significantly reduced postoperative pain scores and opioid consumption after LC. In addition, there were fewer adverse effects in the lidocaine groups. Higher quality RCTs are still required for further research.
Chronic inflammation plays an important role in the mechanisms underpinning the development of anesthesia-induced cognitive dysfunction. However, less is known about how anesthesia causes inflammation. One possibility is that the inflammation is related to alteration of the activity of the alpha 7 nicotinic acetylcholine receptor cholinergic anti-inflammatory pathway. This study analyzed the effect of sevoflurane administration on the cognitive function by using a novel object recognition test and Y-maze test, and on acetylcholinesterase activity and expression in hippocampal tissue by using an acetylcholinesterase assay kit and quantitative real-time PCR. This study also evaluated the effect of alpha 7 nicotinic acetylcholine receptor agonist PNU-282987 and antagonist methyllycaconitine on cognitive function and the level of hippocampal tumor necrosis factor-α in aged rats exposed to sevoflurane anesthesia. We found that 3% sevoflurane significantly impaired cognitive function and increased acetylcholinesterase activity by upregulating its expression in hippocampal tissue. Sevoflurane-induced impairment of cognitive function was significantly rescued by PNU-282987 but aggravated by methyllycaconitine. In addition to impairment of cognitive function, sevoflurane also significantly increased tumor necrosis factor-α level in plasma and hippocampal tissue. Similarly, this sevoflurane-induced change of tumor necrosis factor-α level in rats was antagonized by PNU-282987 but amplified by methyllycaconitine. In conclusion, our data show that the development of inflammation in sevoflurane-induced cognitive decline is associated with the downregulation of alpha 7 nicotinic acetylcholine receptor cholinergic anti-inflammatory pathway in aged rats.
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