Effect of topical ropivacaine on the response to endotracheal tube during emergence from general anesthesia: a prospective randomized double-blind controlled study.

BACKGROUND: The airway reflex such as cough is common accompanied with severe fluctuations of hemodynamics during emergence. This prospective double-blind randomized controlled trial tested the hypothesis that topical ropivacaine may reduce extubation response and postoperative sore throat. METHODS: Fifty-four patients undergoing thyroidectomy were randomly assigned to two groups. The patients in Group R were received 0.75% ropivacaine, which was sprayed on the tracheal mucosa, epiglottis, tongue base, and glottis to achieve uniform surface anesthesia. As control, patients in Group C were received the same volume saline. The primiary outcome was the incidence and grade of cough during peri-extubation. RESULTS: The incidence (34.62% vs. 76.92%, P = 0.002) of cough during extubation were lower in Group R compared to Group C. Meanwhile, the sore throat visual acuity score at 12 h after surgery was lower in Group R than that in Group C (2.00 vs. 3.50, P = 0.040). CONCLUSION: Topical anesthesia with 0.75% ropivacaine before intubation can significantly reduce the incidence of cough during peri-extubation. Meanwhile, it reduced hemodynamic fluctuations and postoperative throat pain without influence patients recovery. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR1800014412 (date of registration January 2018).

Bronchial Blocker Versus Left Double-Lumen Endotracheal Tube for One-Lung Ventilation in Right Video-Assisted Thoracoscopic Surgery.

OBJECTIVE: The aim of this study was to compare the quality of lung deflation of a left-sided double-lumen endotracheal tube (DLT) with a bronchial blocker (BB) for one-lung ventilation in video-assisted thoracic surgery (VATS). DESIGN: A prospective, randomized, clinical study. SETTING: A university-affiliated teaching hospital. PARTICIPANTS: Forty-five adult patients undergoing esophageal tumor surgery using VATS with right lung deflation. INTERVENTIONS: Patients were assigned by a computer-generated randomization sequence to either the left-sided DLT or BB group. The correct positioning of the airway device was confirmed using fiberoptic bronchoscopy. MEASUREMENTS AND MAIN RESULTS: The variables assessed included: (1) time required to correctly place the devices and to achieve lung collapse; (2) the number of times the device malpositioned; (3) the quality of lung deflation as rated by the surgeon; (4) blood pressure and heart rate at baseline (T1), immediately before (T2) and after (T3) and 1 minute (T4) after intubation; (5) the number of patients with hypoxemia (SpO2 < 90%) during the one-lung ventilation (OLV) period; and (6) postoperative hoarseness of voice, sore throat, or pulmonary infection. Of the 45 patients approached for the study, 21 patients in the DLT group and 19 patients in the BB group were analyzed. The time required to place the device in the correct position was similar between the 2 groups. The time to achieve right lung collapse in the BB group was significantly longer (mean difference: 3.232, 95% confidence interval [CI]: 1.993-4.471; p = 0.003). The quality of lung collapse, OLV duration, number of patients with device malposition, and hypoxemia in both groups were similar. There were more patients suffering hoarseness (odds ratio [OR]: 4.85, 95% CI: 1.08-21.76; p = 0.034) or sore throat (OR: 4.29, 95% CI: 1.14-16.18; p = 0.030) in the DLT group, while no patients developed postoperative lung infection in either group. Compared to T1, systolic blood pressure (sBP), diastolic BP (dBP), and heart rate (HR) at T2 in both groups were higher (p < 0.05) in the DLT group. Then, compared to T2, sBP and dBP at T3 and T4 and HR at T3 in the DLT group were higher (p < 0.05). CONCLUSIONS: The results of this study showed that BB is an effective alternative for left one-lung ventilation in right VATS, but requires a longer time to achieve complete lung collapse. Moreover, the use of BB caused less hemodynamic perturbation and can reduce postoperative hoarseness and sore throat.

Endoplasmic reticulum stress is involved in the neuroprotective effect of propofol.

Propofol is a common clinically used intravenous anaesthetic agent with antioxidative property. It has been thought to have neuroprotection in vitro and in vivo. However, the underlying mechanisms remain unclear. Endoplasmic reticulum (ER) stress plays an important role in regulating the signaling pathways concerning cell death and survival. Therefore, we wondered whether the neuroprotective effects of propofol are associated with its regulation on ER stress. In this study, we found that propofol up-regulated BiP and attenuated tunicamycin-induced neural cell death. Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP). We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. However, pretreatment with propofol attenuated the levels of phosphorylated protein kinase receptor-like ER kinase, phosphorylated elF2α, ATF4, and caspase-3, but failed to affect the increase of cleaved ATF6 and XBP1s, induced by tunicamycin. Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3. Meanwhile, knockdown BiP attenuated the protective effects of propofol on the neural cells exposed to tunicamycin. These data suggest that ER stress is involved in the neuroprotection of propofol via differentially regulating the unfolded protein response pathway, in which BiP plays an important role in initiating the adaptive ER stress and inhibiting the apoptotic ER stress.

Peroxisome proliferator-activated receptor-α activation protects against endoplasmic reticulum stress-induced HepG2 cell apoptosis.

Live ischemia-reperfusion injury is associated with endoplasmic reticulum (ER) stress-induced apoptosis. Activation of peroxisome proliferator-activated receptor-α (PPARα) may inhibit hepatocyte apoptosis induced by oxidative stress and protect against liver injury. This study aimed to investigate the effects of PPARα activation, through a specific agonist, on ER stress-induced apoptosis in human liver hepatocellular carcinoma (HepG2) cells. HepG2 cells were challenged with H2O2 and treated with WY14643, a selective PPARα agonist, in the presence or absence of the PPARα antagonist of MK886. Cell viable assay (MTT) and immunostaining were used to evaluate cell viability. The level of apoptotic cell death was quantified through Annexin V/PI staining. Alanine aminotransferase, asparatate aminotransferase, and malondialdehyde levels were measured to determine the presence of cellular injury and oxidative stress. RT-PCR and Western blot analysis were used to detect mRNA and protein expression of PPARα, BiP, and CHOP. Immunofluorescence was utilized to determine the intracellular localization of CHOP. H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus. Compared with cells treated with H2O2 alone, pre-administration of WY14643 increased cell viability, attenuated apoptosis, improved cell function, down-regulated BiP and CHOP expression and inhibited CHOP translocation. The effects of WY14643 were completely abolished using the MK886 antagonist. PPARα activation protects against H2O2-induced HepG2 cell apoptosis. The underlying mechanisms may be associated with its activation to suppress excessive ER stress.