Abstract Background The role of intravenous lidocaine infusion in endoscopic surgery has been previously evaluated for pain relief and recovery. Recently, it has been shown to reduce postoperative pain and opioid in patients undergoing endoscopic submucosal dissection. Similar to endoscopic submucosal dissection, operative hysteroscopy is also an endoscopic surgical procedure within natural lumens. The present study was a randomized clinical trial in which we evaluated whether intravenous lidocaine infusion would reduce postoperative pain in patients undergoing hysteroscopic surgery. Objective To evaluate whether intravenous lidocaine infusion could reduce postoperative pain in patients undergoing operative hysteroscopy. Methods Eighty-five patients scheduled to undergo elective hysteroscopy were randomized to receive either an intravenous bolus of lidocaine 1.5 mg.kg-1 over 3 minutes, followed by continuous infusion at a rate of 2 mg.kg-1. h-1 during surgery, or 0.9% normal saline solution at the same rate. The primary outcome was to evaluate postoperative pain by Visual Analog Scale (VAS). Secondary outcomes included remifentanil and propofol consumption. Results In the lidocaine group, the VAS was significantly lower at 0.5 hour (p = 0.008) and 4 hours (p = 0.020). Patients in the lidocaine group required less remifentanil than patients in the control group (p < 0.001). However, there was no difference between the two groups in the propofol consumption. The incidence of throat pain was significantly lower in the lidocaine group (p = 0.019). No adverse events associated with lidocaine infusion were discovered. Conclusion Intravenous lidocaine infusion as an adjuvant reduces short-term postoperative pain in patients undergoing operative hysteroscopy.

Abstract Purpose: To investigate the influence of lycium barbarum polysaccharides (LBP), a functional derivative from lycium barbarum, on septic kidney injury. Methods: The SD male rats were randomly divided into 8 groups. The concentration of IL-1β, IL-6, IL-8, TNF-α, NF-κB and ROS, in kidney cortex homogenates after 12 h treatments were determined by enzyme-linked immunosorbent assay and ROS test kit, respectively. Morphology observation of kidney tissue was conducted with HE staining. The mRNA and protein expression levels of Nrf2, HO-1, NQO1, NF-κB, and Keap1 in kidney tissues were determined by qRT-PCR and Western blot, respectively. Results: LPS treatment significantly increased the oxidative stress. After LBP treatment, the ROS content reduced significantly in a dose-depend manner. However, the levels of HO-1, NQO1 and Nrf2 as molecular elements that respond to oxidative stress were further increased. Also, administration of LBP increased the levels of NF-κB and Keap1, and decreased the levels of Nrf2 in the Keap 1-Nrf2∕ARE signaling pathway. By administrating the brusatol, the inhibition of Nrf2 enhanced the expression of NF-κB, inhibits the antioxidant responses, and further reverse the protective effect of LBP on the LPS induced septic kidney injury. Conclusion: Lycium barbarum polysaccharides can reduce inflammation and activate the antioxidant responses via regulating the level of pro-inflammatory cytokines and the Keap1-Nrf2/ARE signaling pathway.

PURPOSE: To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. METHODS: Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. RESULTS: I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). CONCLUSION: Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats.