Comparison of the Analgesic Effects of Intravenous Infusion of Dexmedetomidine Versus Bilateral Superficial Cervical Plexus Block After Thyroidectomy: A Randomized Controlled Trial.

OBJECTIVES: Dexmedetomidine (DEX) is widely used in clinical practice because of its safety and effectiveness. Superficial cervical plexus block (SCPB) can reduce pain in thyroid surgery. The objective of this study was to investigated whether intravenous DEX has an equivalent analgesic effect and patients' satisfaction to SCPB for thyroid surgery. MATERIALS AND METHODS: Ninety patients who had been scheduled for thyroidectomy under general anesthesia with endotracheal intubation were randomly divided into 3 groups. Group D: DEX was administered intravenously at an initial dose of 1 µg/kg over 10 minutes; then induction and endotracheal intubation performed, and then a continuous intravenous infusion of DEX was administered at a rate of 0.4 µg/kg/h until 30 minutes before the end of surgery. Group B: ultrasound-guided bilateral SCPB was performed, with 10 mL of 0.375% ropivacaine injected on each side. Group C: intravenous saline was administered at the same rate and dose as in group D. Patients' perioperative status, visual analog scale scores, complications and patients' satisfaction were recorded. RESULTS: The pain at rest at 1 hour after extubation and the movement-evoked pain within 24 hours after extubation were significantly lower in groups D and B than in group C. Patients' satisfaction was significantly higher in groups D and B than in group C. There was no difference in pain at rest, movement-evoked pain and patients' satisfaction between group D and B. CONCLUSIONS: Perioperative intravenous infusion of DEX can effectively reduce wound pain after thyroidectomy, and the analgesic effect is equivalent to that of bilateral SCPB.

NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p.

BACKGROUND AND AIM: Acute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI. MATERIALS AND METHODS: A septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay. RESULTS: NEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p. CONCLUSION: Depletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.