Sepsis-Associated Encephalopathy (SAE) is common in sepsis patients, with high mortality rates. It is believed that neuroinflammation is an important mechanism involved in SAE. High mobility group box 1 protein (HMGB1), as a late pro-inflammatory factor, is significantly increased during sepsis in different brain regions, including the hippocampus. HMGB1 causes neuroinflammation and cognitive impairment through direct binding to advanced glycation end products (RAGE) and Toll-like receptor 4 (TLR4). Electroacupuncture (EA) at Baihui (GV20) and Zusanli (ST36) is beneficial for neurological diseases and experimental sepsis. Our study used EA to treat SAE induced by lipopolysaccharide (LPS) in male Sprague–Dawley rats. The Y maze test was performed to assess working memory. Immunofluorescence (IF) and Western blotting (WB) were used to determine neuroinflammation and the HMGB1 signaling pathway. Results showed that EA could improve working memory impairment in rats with SAE. EA alleviated neuroinflammation by downregulating the hippocampus’s HMGB1/TLR4 and HMGB1/RAGE signaling, reducing the levels of pro-inflammatory factors, and relieving microglial and astrocyte activation. However, EA did not affect the tight junctions’ expression of the blood–brain barrier (BBB) in the hippocampus.
Background Hypokalemia is a common form of electrolyte disorder, which has a higher incidence in hospitalized patients and is closely related to perioperative complications and prognosis. Due to decreased skeletal muscle mass which causes total body potassium reduction, and increased comorbidities, the elderly are more susceptible to hypokalemia. Objective To investigate preoperative hypokalemia in elderly patients and its effect on postoperative complications. Methods Data were retrospectively collected from the elderly patients who underwent elective surgery from April 2018 to March 2019 and had preoperative blood gas data available. Patients, with age 60 to 100 years, were divided into hypokalemia group (potassium level < 3.5 mmol/L) and normokalemia group (potassium level between 3.5 and 5.5 mmol/L) according to preoperative blood gas analysis. Hypokalemia can be divided into mild (potassium level 3.0 to 3.5 mmol/L), moderate (potassium level 2.5 to 3.0 mmol/L) and severe (potassium level < 2.5 mmol/L), respectively. The risk factors of preoperative hypokalemia and its impact on postoperative complications and prognosis were primary outcomes. Secondary outcomes included postanesthesia care unit (PACU) stay time and hospital length of stay (LOS). Results Of 987 participants, 436 (44.17%) developed preoperative hypokalemia, among them 357 (81.88%) mild, 87 (16.74%) moderate and 6 (1.38%) severe. Multivariate logistic regression showed that female gender (OR, 1.851; 95% CI, 1.415–2.421), pre-existing hypokalemia at admission (OR, 4.498; 95% CI, 2.506–8.071), and oral laxative twice or more (OR, 1.823; 95% CI, 1.266–2.624) are risk factors of preoperative hypokalemia. Gynecological and biliopancreatic surgery were more common in hypokalemia group than normokalemia group (P < 0.001, P < 0.05). There was no significant difference in postoperative complications, PACU stay time, LOS, and 30-day mortality between the two groups (all P > 0.05). Conclusions Female gender, pre-existing hypokalemia at admission, and oral laxative twice or more are independent risk factors for preoperative hypokalemia in elderly patients. However, postoperative complications and 30-day mortality were not increased, which may be related to monitoring blood gas analysis and prompt correction of potassium levels during surgery.
Objective To evaluate the analgesic efficacy of quadratus lumborum block (QLB) in adults undergoing nephrectomy. Design Systematic review and meta-analysis. Patients Adult patients (≥ 18 years) received nephrectomy under general anesthesia. Methods We searched PubMed, Embase, the Cochrane Library, and Web of Science on January 10, 2022, including randomized controlled trials (RCTs) that evaluated the analgesic efficacy of QLB for patients undergoing nephrectomy. Results A total of 12 RCTs (N = 821 patients) were included in the study. Compared with the non-block, single-shot QLB reduced the postoperative opioid consumption (mean difference [MD], -8.37 mg intravenous morphine equivalent; 95% CI, -12.19 to -4.54 mg) and pain scores at 2 h, 6 h, 12 h, and 24 h at rest and during movement after nephrectomy. Single-shot QLB also prolonged the time to first analgesic request (MD, 6.44 h; 95% CI, 2.23 to 10.65 h), and shortened the length of hospital stay (MD, -0.32 d; 95% CI, -0.55 to -0.09 d) and decreased the incidence of postoperative nausea and vomiting (risk ratio, 0.48; 95% CI, 0.36 to 0.65). Compared with continuous epidural anesthesia, repeated QLB may provide comparable postoperative analgesic benefits. Conclusions Single-shot QLB provided a statistically significant, but clinically-small improvement in postoperative analgesia and recovery for patients undergoing nephrectomy. The QLB would be beneficial as part of multimodal analgesia. Future research may need to determine which approach of QLB is superior for postoperative analgesia after nephrectomy.
Postoperative neurocognitive dysfunction (PND) is a common postoperative complication. Autophagy is correlated with the pathogenesis of PND. This study investigated the potential role of autophagy in the neuroprotection of Dexmedetomidine (Dex) pretreatment in PND. The PND rat model was established by abdominal surgery. The cognitive function of rats was evaluated by Y-maze 3 days after surgery. Nissl staining assessed postoperative hippocampal damage. Immunofluorescence detected the expression of microglial activation (Iba-1) and autophagy-related protein (LC3B) in hippocampal tissues. Western blot detected the autophagy-related protein expression (Beclin 1, LC3B, and p62), proinflammatory cytokines, and the protein activation of the LKB1/AMPK/ULK-1 signaling pathway. RT-PCR quantified the expression of IL-1β, TNF-α, and IL6. In this study, we found Dex pretreatment improved spatial memory function impairment and reduced abdominal surgery-induced hippocampal tissue damage. Dex pretreatment significantly increased the expression of Beclin 1 and LC3 II/I, and decreased the expression of p62 in the hippocampus after surgery. Furthermore, Dex effectively inhibited microglial activation and proinflammatory cytokines by enhancing autophagy in the hippocampus. Pretreatment with 3-MA, an autophagy inhibitor, the inhibitory effect of Dex on postoperative neuroinflammation was significantly weakened. We further demonstrated that Dex suppressed surgery-induced neuroinflammation by activating the LKB/AMPK/ULK1 signaling pathway. In conclusion, our study indicated that Dex inhibited hippocampal neuroinflammation and ameliorated PND by enhancing autophagy after surgery in rats, which was related to the LKB1/AMPK/ULK1 signaling pathway. These findings provide a potential therapeutic prospect for PND.
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