ABSTRACT
Objective:To evaluate the efficacy of continuous infusion of lidocaine via urinary catheter for postoperative analgesia in patients undergoing urological surgery.Methods:Forty male American Society of Anesthesiologists physical status Ⅱ or Ⅲ patients, aged 65-75 yr, with body mass index of 18-25 kg/m 2, scheduled for elective percutaneous nephrolithotomy, were divided into 2 groups ( n=20 each) using a random number table method: continuous infusion of lidocaine through urinary catheter group (group L) and patient controlled intravenous analgesia (PCIA) group (group PCIA). All the patients underwent total intravenous anesthesia, and a matched type of sterile urethral irrigation catheter was inserted after the operation.In group L, 0.5% lidocaine was continuously infused at a rate of 5 ml/h via the urinary catheter, while the equal volume of 0.9% normal saline was continuously infused via the urinary catheter, and PCIA was connected in group PCIA.PCIA solution contained sufentanil 125 μg (diluted to 250 ml in normal saline), and the PCA pump was set up with a 5 ml bolus dose, a 15 min lockout interval and background infusion at a rate of 5 ml/h.When visual analogue score was>4, sufentanil 0.05 μg/kg was injected intravenously as rescue analgesic.The development and severity of catheter-related bladder discomfort (CRBD) were recorded immediately at the end of the operation (T 1), and at 6 h (T 2), 24 h (T 3) and 48 h (T 4) after the operation, respectively.Riker sedation-agitation scale (SAS) score was recorded at T 1, 2, and QoR-9 scale was recorded at T 3, 4.The concentrations of serum cortisol (Cor), norepinephrine (NE), epinephrine (E) and blood glucose (Glu) were measured by enzyme linked immunosorbent assay.First off-bed time, exhaust time, length of hospital stay after surgery, and the requirement for rescue analgesia and adverse reactions (nausea and vomiting, respiratory depression, hypotension, skin itching) within 48 h after the operation were recorded. Results:Compared with group PCIA, the incidence of CRBD and the severity were significantly decreased at T 1-4, SAS score was decreased at T 1, 2, QoR-9 score was increased at T 3, 4, Cor, NE, E and Glu concentrations were decreased at T 1-4, the incidence of postoperative rescue analgesia was decreased, first off-bed time, exhaust time and length of hospital stay after surgery was shortened, and the incidence of postoperative nausea and vomiting, respiratory depression, hypotension, skin itching was decreased in group L ( P<0.05). Conclusion:Continuous infusion of lidocaine through the urinary catheter can provide good postoperative analgesia, reduce postoperative stress response and adverse reactions, and facilitate early postoperative recovery in patients undergoing urological surgery.
ABSTRACT
In the original publication the grant number is incorrectly published. The correct grant number should be read as "17140901600". The corrected contents are provided in this correction article. This work was partially supported by grants from the National Natural Science Foundation of China (Nos. 81670470 and 81600149), a grant from the Shanghai Municipal Commission for Science and Technology (17140901600, 18411953500 and 15JC1400201) and a grant from National Key Research and Development Program (2016YFC0905100).
ABSTRACT
The cell type that normally limits the inflammatory and atherosclerotic process is the vascular endothelial cell (EC) that can be regulated by proinflammatory and various stresses. Toll-like receptor-4 (TLR4) plays an important role in the pathogenesis of atherosclerosis, in part, by activating apoptosis signal-regulating kinase 1 (ASK1) to initiate the activation of MAP kinases pathways and the expression of inflammatory genes. In the present study, we test the hypothesis that AGI-1067 acts as an anti-inflammatory agent by inhibiting the activation of ASK1 in human EC. Pretreatment of human aortic endothelial cells with AGI-1067 inhibits TLR4 ligand (LPS)-induced activation of ASK1 and the downstream p38 and c-Jun N-terminal kinase (JNK) MAP kinases. LPS dissociates two endogenous inhibitors thioredoxin-1 (Trx1) and 14-3-3 from ASK1, leading to ASK1 autoactivation. Interestingly, AGI-1067 inhibits the dissociation of Trx1, but not 14-3-3, from ASK1. However, inhibition of Trx1 dissociation from ASK1 by AGI-1067 is sufficient to suppress LPS-mediated phosphorylation of the transcription factors c-Jun and activating transcription factor 2, and inhibit LPS-induced inflammatory genes including vascular cell adhesion molecule 1, E-selectin, IL-6 and monocyte chemoattractant protein 1. Our findings suggest that AGI-1067 as a unique ASK1 inhibitor to inhibit TLR4-mediated ASK1 activation, contributing to its anti-inflammatory properties.
