目的 探讨乳腺癌改良根治术中超声引导下胸神经阻滞的应用效果.方法 选取乳腺癌改良根治术患者96例,按随机数字表法分为实验组(n=48)与对照组(n=48).对照组采用超声引导下胸椎旁神经阻滞,实验组采用超声引导下胸神经阻滞.对比2组麻醉前(T1)、手术10 min(T2)、手术30 min(T3)、术后即刻(T4)的应激反应[收缩压(SBP)、心率(HR)]、视觉模拟评分法(VAS)评分、不良反应发生率.结果 T2、T3、T4实验组SBP、HR水平较对照组低,且实验组波动幅度较对照组小(P<0.05).术后3 h、术后6 h、术后12 h实验组VAS评分较对照组低(P<0.05).实验组不良反应发生率为4.17％(2/48),较对照组的20.83％(10/48)低(P<0.05).结论 乳腺癌改良根治术中应用超声引导下胸神经阻滞可减轻应激反应,维持血流动力学稳定,减轻术后疼痛,降低不良反应发生率.

Dexmedetomidine (Dex) plays protective effects on brain ischemia–reperfusion (I/R) injury, but its mechanism remains unclear. In this study, we aimed to investigate whether Dex protects neurons against I/R injury by activating SIRT3 mediated autophagy. The oxygen glucose deprivation-reperfusion (OGD/R) model was constructed in HT22 cells. Different doses of Dex (50 ng/mL, 100 ng/mL and 500 ng/mL) were treated to observe the changes of autophagy and SIRT3 expression. Further, the mimic of SIRT3 and SIRT3 inhibitor were used to analyze the effects of Dex on the SIRT3 expression in HT22 cells. Additionally, the autophagy inhibitor and AMPK inhibitor were used to analyze the effects of Dex on SIRT3 mediated autophagy. The cells viability, oxidative stress and ATP were observed using assay kits. The mitochondrial membrane potential (MMP) and death were analyzed by flow cytometry. The degree of autophagy was observed by acridine orange staining. Western blotting was used to analyze the expression of autophagy related proteins and AMPK/mTOR pathway related proteins. After Dex treatment, the OGD/R induced cell injury was significantly improved through decreasing the levels of LDH and H2O2, increasing levels of ATP and MMP. Furthermore, Dex increased the degree of autophagy and expression of SIRT3 in OGD/R injured cells. Through overexpression of SIRT3, the OGD/R induced cell injury was also clearly improved. But the SIRT3 inhibitor or autophagy inhibitor covered the roles of Dex. Additionally, AMPK inhibitor played an opposite role compared with the effects of Dex treatment. From this study, the protection mechanism of Dex on neurons I/R injury might related to the activation of SIRT3 mediated autophagy.

肌间沟臂丛神经阻滞是一种操作方便及具有确切麻醉效果的神经阻滞技术,主要通过在臂丛神经干周围注射局麻药物来实现,常常应用于上肢手术的麻醉[1].盲探法是传统的操作方法,该技术主要依据解剖定位来实施,过于依赖术者的个人经验,且对于肥胖患者定位的难度大增,更容易导致阻滞失败及发生血管、神经损伤等并发症.近年来,神经刺激仪引导的肌间沟臂丛神经阻滞在临床上应用较为广泛,其原理在于电流对神经支配区域的肌肉进行刺激引起肌肉颤动,进而指导阻滞的进行[2].但是该技术仍然属于盲探性操作的范畴,不能在可视下进行精准操作.超声引导下神经阻滞技术的应用弥补了既往盲探法的不足,可以精准定位且操作及局麻药的扩散均可进行直接观察.本研究以上肢手术肥胖患者为研究对象,对比了超声与神经刺激仪引导肌间沟臂丛神经阻滞的应用效果,现报告如下.

目的:评价改良鼻咽通气道用于全麻术后拔管患者呼气末二氧化碳分压(PetCO2)监测的效果.方法:将120例全麻术后拔管患者分为鼻咽通气道组(P组)和鼻氧管组(N组),每组60例.吸入氧流量为0 L/min时,采集两组患者的PetCO2和动脉血二氧化碳分压(PaCO2)数据,进行相关性和一致性分析.调节吸入氧流量至2、4、6 L/min,采集两组患者不同氧流量下的PetCO2数据.结果:氧流量为0 L/min时,两组患者PetCO2和PaCO2均呈正相关(P组:r=0.846,P<0.001;N组:r=0.794,P<0.001);P组PaCO2和PetCO2差值为(0.89±0.31)kPa,95％一致性界限为0.29～1.49 kPa;N组PaCO2和PetCO2差值为(0.95±0.33)kPa,95％一致性界限为0.30～1.60 kPa.两组差值比较,差异无统计学意义(P=0.308).随着氧流量由0 L/min增至6 L/min,P组PetCO2无变化,N组PetCO2逐渐降低(P<0.001).结论:改良鼻咽通气道用于全麻术后拔管患者PetCO2监测,有较好的准确性和稳定性.

BACKGROUND:The aim of the study was to explore the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity.METHODS:Mouse DRG neurons were cultured in vitro and treated with bupivacaine to establish a neurotoxicity model. Caspase3 activity, cell viability, and TUNEL assays were analyzed to assess the role of lincRNA PADNA. A dual-luciferase reporter assay was used to determine the binding target of lincRNA PANDA.RESULTS:The expression of lincRNA PADNA was significantly increased with increasing concentrations of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA increased caspase3 activity and inhibited cell viability. Western blot analysis showed that knockdown of lincRNA PADNA promoted cleaved caspase3 levels. We also revealed that lincRNA PADNA may bind with miR-194. Knockdown of miR-194 rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidence that the lincRNA PADNA/miR-194/FBXW7 axis plays an important role in the neurotoxicity process.CONCLUSION:We performed comprehensive experiments to verify the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Our study provides new evidence and clues for the prevention of neurotoxicity.

Purpose: Non-small cell lung cancer (NSCLC) accounts for more than 80% of lung cancer cases and remains the primary cause of cancer-related deaths worldwide. Fentanyl is a commonly utilized anesthetic during the process of tumor resection, and exhibits inhibitory effects on the progression of numerous cancer types, including pancreatic cancer, colorectal cancer and gastric cancer. However, the effects of fentanyl on the cell viability and invasion of NSCLC has not been investigated. Current study aimed to investigate the effects and the mechanisms underlying the effects of fentanyl on NSCLC. Methods: The expression of mu-opioid receptor (MOR) was proved by flow cytometry. The expression of microRNA-331-3p (miR-331-3p) and histone deacetylase 5 (HDAC5) in NSCLC tissues and cell lines are evaluated by reverse transcription-quantitative PCR (RT-qPCR) and Western blot, respectively. Cell viability and invasion are measured by cell counting kit-8 (CCK8) assay and transwell assay, respectively. The interaction between miR-331-3p and 3'-untranslated region (UTR) of HDAC5 is predicted by TargetScan 7.1 (hap://www.targetscan. orglvert_71/), validated by dual luciferase assay, RT-qPCR and Western blot. Results: There was lower miR-331-3p expression and higher HDAC5 expression in NSCLC cell lines A549 and CALU-1 compared with BEAS-2B, which was reversed by fentanyl administration. miR-331-3p targeted 3'-UTR of HDAC5 in NSCLC cell lines A549 and CALU-1. miR-331-3p inhibitor partially abrogated the inhibitory effects of fentanyl on NSCLC cell viability and invasion by targeting HDAC5. In addition, there was higher HDAC5 expression and lower miR-331-3p expression in tumor tissues which were isolated from patients with NSCLC compared to the adjacent normal tissues, and miR-331-3p was negatively correlated with HDAC5 in NSCLC tumor tissues. Conclusion: Fentanyl inhibits the viability and invasion of NSCLC cells by induction of miR-331-3p and reduction of HDAC5.