Comparison of ultrasound-guided lumbar plexus block and continuous adductor canal nerve block in total hip arthroplasty / 中国医师进修杂志

Objective:To compare the application value of ultrasound-guided lumbar plexus block (LPB) and continuous adductor canal nerve block (ACNB) in total hip arthroplasty (THA), and to explore the anesthesia scheme of THA.Methods:A prospective randomized controlled trial was used. Ninety patients who received THA admitted to in Lishui People′s Hospital from March 2019 to February 2022 were selected as the study subjects. According to the random number table method, 90 patients were divided into the test group and the control group, with 45 patients in each. The control group received LPB + general anesthesia, and the test group received ACNB + general anesthesia. By evaluating the hemodynamic parameters heart rate (HR) and mean arterial pressure (MAP) at the time of entry (T 1), osteotomy (T 2), prosthesis implantation (T 3) and immediately after surgery (T 4); the pain degree visual analogue score (VAS) at 6 h (S 1), 12 h (S 2), 24 h (S 3), 48 h (S 4) after awakening; the dosage of anesthetic drugs, the anesthetic effects of LPB and ACNB in THA were compared. Results:From T 2 to T 4, HR of patients in the two groups had a trend of increase: (85.24 ± 4.26) times/min vs. (86.13 ± 4.86) times/min, (83.82 ± 5.11) times/min vs. (85.16 ± 3.56) times/min and (81.64 ± 4.32) times/min vs. (82.24 ± 4.62) times/min, while MAP was in a downward trend: (86.54 ± 4.25) mmHg (1 mmHg = 0.133 kPa) vs. (85.35 ± 4.66) mmHg, (86.15 ± 3.92) mmHg vs. (84.86 ± 4.13) mmHg and (90.65 ± 5.25) mmHg vs. (92.12 ± 4.62) mmHg. The difference at different time points was statistically significant ( P<0.05). There was no statistically significant difference in HR, MAP and change trend between the two groups at different time ( P>0.05). The VAS score of the two groups increased from S 2 time point, and the difference between different time points was statistically significant ( P<0.05). The rising trend of VAS score in the test group was lower than that in the control group, and the VAS score at different time points was lower than that in the control group ( P<0.05). The dosage of sufentanil used in the test group was less than that in the control group: (114.37 ± 16.61) μg vs. (131.36 ± 18.31) μg, and the number of press of analgesia pump was less than that in the control group: 6.00 (5.00, 6.50) times vs. 8.00 (7.00, 9.00) times ( P<0.05). Conclusions:Ultrasound-guided LPB and ACNB could maintain hemodynamic stability in THA. Especially, ACNB could play an analgesic role within 48 h after THA and reduce the dosage of analgesic drugs.

Dexmedetomidine reduces dextran sulfate sodium (DSS)-induced NCM460 cell inflammation and barrier damage by inhibiting RhoA/ROCK signaling pathway

Objective This study investigated the role of dexmedetomidine (DEX) in dextran sulfate sodium (DSS)-induced NCM460 cells.Material and Methods The viability and apoptosis of NCM460 cells treated with DEX with or without DSS were detected by CCK-8 and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay. The level of inflammatory factors and expression of inflammation-related proteins, tight junction proteins and Ras homolog gene family, member A/Rho-associated coiled-coil containing protein kinase (RhoA/ROCK) signaling-related proteins in NCM460 cells treated with DEX and/or U46619 (RhoA/ROCK agonist) and/or DSS were detected by the respective enzyme-linked immunosorbent assay (ELISA) kits and Western blot analysis. The permeability of NCM460 monolayers was examined with transepithelial electrical resistance (TEER) assay.Results DEX had no effect on NCM460 cell viability. However, DEX improved the viability and barrier damage and suppressed the apoptosis and inflammation of DSS-induced NCM460 cells. Correspondingly, the expression of inflammation-related proteins was reduced and the expression of tight junction proteins was increased in DSS-induced NCM460 cells after treatment with DEX. In addition, RhoA/ROCK signaling was activated in NCM460 cells induced by DSS, which was suppressed by DEX. The protective effects of DEX on DSS-indued NCM460 cells were reversed by U46619 (AU)

Role of PI3K/Akt signaling pathway and autophagy in reduction of adriamycin-induced myocardial injury by sevoflurane in rats / 中华麻醉学杂志

Objective To evaluate the role of phosphatidylinositol 3-kinase/protein-serine-threonine kinases (PI3K/Akt) signaling pathway and autophagy in reduction of adriamycin-induced myocardial injury by sevoflurane in the rats.Methods Thirty-six healthy male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 6 groups (n =6 each) using a random number table:control group (group C),adriamycin-induced myocardial injury group (group Dox),sevoflurane group (group Sev),LY294002 inhibitor group (group LY),solvent control group (group dimethyl sulfoxide [DMSO]),and 3-MA inhibitor group (group 3-MA).Adriamycin 4 mg/kg was injected intraperitoneally once a week for 3 weeks in all the groups except group C.The rats were mechanically ventilated for 2 h in C and Dox groups.The rats inhaled 2.4％ sevoflurane for 2 h in group Sev.In group LY,0.3 mg/kg LY294002 was injected via the tail vein at 10 min before anesthesia,and the rats inhaled 2.4％ sevoflurane for 2 h.In group DMSO,the equal volume of DMSO was injected,and the rats inhaled 2.4％ sevoflurane for 2 h.After the blood samples were collected from the heart,the rats were sacrificed,and myocardial specimens were obtained for determination of cardiac troponin Ⅰ (cTnI) concentrations in serum (by enzyme-linked immunosorbent assay),expression of total Akt (t-Akt),phosphorylated Akt (p-Akt),mammalian target of rapamycin (mTOR),phosphorylated mTOR (p-mTOR) and autophagy marker microtubule-associated protein light chain 3 Ⅱ (LC3 Ⅱ) (by Western blot),and cell apoptosis (by TUNEL).Apoptosis index (AI) was calculated.Results Compared with group C,the expression of p-Akt and p-mTOR was significantly down-regulated,and the expression of LC3 Ⅱ,AI,and serum cTnI concentration were significantly increased in the other five groups (P＜ 0.05).Compared with group Dox,the expression of p-Akt and p-mTOR was significantly up-regulated,and the expression of LC3 Ⅱ,AI,and serum cTnI concentration were significantly decreased in group Sev (P＜0.05).Compared with group Sev,the expression of p-Akt and p-mTOR was significantly down-regulated,and the expression of LC3 Ⅱ,AI,and serum cTnI concentration were significantly increased in group LY,and the expression of LC3 Ⅱ was significantly down-regulated,and serum cTnI concentrations were significantly decreased in group 3-MA (P＜0.05).Conclusion Sevoflurane can activate PI3K/Akt signaling pathway and inhibit autophagy,thus reducing adriamycin-induced myocardial injury in rats.