ABSTRACT
BACKGROUND: This study compared the effectiveness of nalmefene and fentanyl in reducing the incidence and severity of etomidate-induced myoclonus. METHODS: One hundred fifty patients were randomized to receive 0.25ug/kg of nalmefene, 1ug/kg of fentanyl, or the same volume of normal saline 3 minutes prior to etomidate-induced anesthesia. The primary observational indexes were the severity level and incidence of etomidate-induced myoclonus, and the secondary observational index included blood pressure, heart rate, and the incidence of adverse effects from anesthesia induction to resuscitation, such as cough, chest wall rigidity, dizziness, nausea, pain after awakening, and intraoperative awareness. RESULTS: The incidence of myoclonus was significantly lower in the nalmefene group (8.0%) than in the fentanyl group (32.0%) (P = .003) and in the normal saline group (72.0%) (P = .000). The severity level of myoclonus in the nalmefene group was significantly lower than the fentanyl group (P = .001) and normal saline group (P = .000). Meanwhile, the incidences of cough and chest wall rigidity during anesthesia induction were significantly lower in the nalmefene group compared with the fentanyl group (P = .003, P = .027). There were no statistically significant differences in heart rate and mean arterial pressure among the 3 gruops (P > .05). There was no difference in the incidence of adverse effects among the 3 groups during recovery from anesthesia (P > .05). CONCLUSION: Intravenous injection of 0.25ug/kg of nalmefene 3 minutes prior to etomidate is more effective in preventing etomidate-induced myoclonus during general anesthesia than 1ug/kg of fentanyl.
Subject(s)
Drug-Related Side Effects and Adverse Reactions , Etomidate , Myoclonus , Humans , Etomidate/adverse effects , Cough , Myoclonus/chemically induced , Myoclonus/prevention & control , Saline Solution , Anesthesia, General , Fentanyl/adverse effectsABSTRACT
Background: Surgical resection is the most effective treatment for lung cancer, but it can also lead to adverse stress reactions in the body. The minimization of lung function damage caused by one-lung ventilation and inflammatory reactions caused by surgery are new challenges faced by the field of anesthesiology. Dexmedetomidine (Dex) has been found to be effective in improving perioperative lung function. In this study, we aimed to conduct a systematic review and meta-analysis to examine the effect of Dex on inflammation and pulmonary function after thoracoscopic surgery for lung cancer. Methods: A computer-based search was performed to retrieve controlled trials (CTs) about the effects of Dex on inflammation and lung function after thoracoscopic surgery for lung cancer from the databases of PubMed, Embase, Cochrane Library, and Web of Science. The time period for retrieval was set from inception to 1 August 2022. The articles were strictly screened according to the inclusion and exclusion criteria, and data analysis was conducted using the software Stata 15.0. Results: A total of 11 CTs were included, involving 1,026 patients overall, with 512 assigned to the Dex group and 514 to the control group. The meta-analysis showed that after Dex treatment, the inflammatory factors of patients with lung cancer who underwent radical resection were all decreased: interleukin-6 (IL-6) [standardized mean difference (SMD) =-2.09; 95% confidence interval (CI): -3.03, -1.14; P=0.003], interleukin-8 (IL-8) (SMD =-1.12; 95% CI: -1.54, -0.71; P=0.001), and tumor necrosis factor-α (TNF-α) (SMD =-2.04; 95% CI: -3.24, 0.84; P=0.001). The pulmonary function of the patients was also improved: forced expiratory volume in the first second (FEV1) (SMD =0.50; 95% CI: 0.24, 0.76; P=0.003), and partial pressure of oxygen (PaO2) (SMD =1.00; 95% CI: 0.40, 1.59; P=0.001). However, there was no significant difference between the two groups regarding adverse reactions [relative risk (RR) =0.68; 95% CI: 0.41, 1.14; P=0.27]. Conclusions: In summary, the use of Dex in lung cancer patients after radical surgery can reduce serum inflammatory factors, and this may play an important role in postoperative inflammatory reaction and improving lung function.
ABSTRACT
OBJECTIVE: To reveal the effects and related mechanism of cisatracurium on colorectal cancer (CRC) development. METHODS: HCT116 and SW480 cells were treated with various concentrations of cisatracurium or transforming growth factor-ß (TGF-ß). Chemokine C-X-C-Motif Receptor 4 (CXCR4) was overexpressed and let-7a-5p was silenced in cells by transfection with pcDNA3.1-CXCR4 or let-7a-5p inhibitor. Cell Counting Kit-8 (CCK-8) assay measured cell viability, and transwell and wound healing assays evaluated cell invasion and migration, respectively. The expression levels of let-7a-5p and CXCR4 were measured using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Western blotting was conducted to test the levels of CXCR4, TGF-ß/SMAD2/3 signalling and metastasis-related proteins. A tumour xenograft assay was performed to assess tumour growth. RESULTS: Cisatracurium treatment suppressed the viability and metastasis of HCT116 and SW480 cells in a concentration-dependent manner, whereas activating TGF-ß/SMAD2/3 signalling significantly reversed these effects. Cisatracurium treatment markedly reduced CXCR4 expression by inhibiting TGF-ß/SMAD2/3 signalling. Besides, let-7a-5p was identified as a target of CXCR4 and could be upregulated by cisatracurium. Both CXCR4 overexpression and let-7a-5p knockdown alleviated the biological roles of cisatracurium in CRC cells. Moreover, a tumour xenograft assay further confirmed that cisatracurium inhibited tumour growth and metastasis by increasing let-7a-5p expression. CONCLUSION: Cisatracurium suppressed the viability, metastasis and tumour growth of CRC by regulating the CXCR4/let-7a-5p axis via inhibiting TGF-ß/SMAD2/3 signalling. These findings provide a theoretical basis for the role of cisatracurium in the prognosis of CRC patients.
