Objective:To investigate the effects of dexmedetomidine combined with esketamine on postoperative analgesia, immune function and inflammatory response in patients undergoing radical mastectomy.Methods:108 patients with breast cancer who received radical mastectomy in Breast Surgery Department, Shanxi Cancer Hospital from Apr. 2022 to Apr. 2024 were divided into the control group (n=54, esketamine) and the observation group (n=54, esketamine + dexmedetomidine) by random number table method. The postoperative recovery, analgesic effect, immune function indexes and inflammatory factors were compared between the two groups, and the occurrence of adverse reactions were recorded.Results:The number of postoperative analgesic pump compression in the observation group was less than that in the control group ( t = 6.60, P<0.05); There was no significant difference between the two groups in the proportion of patients with additional analgesic drugs, postoperative wakefulness-eye opening time or 15-item quality of recovery (QoR-15) scale ( χ2=0.32, t=1.32, 1.15, P>0.05); The observation group had lower VAS scores at 30min (T1), 4 h (T2), 8 h (T3) and 12 h (T4) after surgery ( t=4.82, 6.53, 14.01, 12.87, P<0.05); At T1, T2, T3 and T4, peripheral helper T cells (Th) 1 and Th1/Th2 in observation group were higher, while Th2 was lower ( t=3.98, 4.62, 4.12, 8.52, 3.81, 9.47, 13.98, 9.53, 4.44, 4.50, 4.31, 5.45, all P<0.05); The observation group had lower tumor necrosis factor -α (TNF-α), interleukin-6 (IL-6) at T1, T2, T3 and T4, while higher IL-2 ( t=2.46, 2.99, 2.29, 3.05, 2.85, 3.64, 4.70, 2.51, 3.17, 3.74, 3.24, 2.79, all P<0.05); The incidence of adverse reactions between the two groups showed no significant difference ( χ2=2.31, P>0.05) . Conclusion:Dexmedetomidine combined with esketamine analgesia regimen can significantly improve the analgesic effect after radical mastectomy, reduce postoperative inflammatory response, and effectively protect postoperative immune function of patients, with certain safety.

Objective:To investigate the effects of dexmedetomidine combined with esketamine on postoperative analgesia, immune function and inflammatory response in patients undergoing radical mastectomy.Methods:108 patients with breast cancer who received radical mastectomy in Breast Surgery Department, Shanxi Cancer Hospital from Apr. 2022 to Apr. 2024 were divided into the control group (n=54, esketamine) and the observation group (n=54, esketamine + dexmedetomidine) by random number table method. The postoperative recovery, analgesic effect, immune function indexes and inflammatory factors were compared between the two groups, and the occurrence of adverse reactions were recorded.Results:The number of postoperative analgesic pump compression in the observation group was less than that in the control group ( t = 6.60, P<0.05); There was no significant difference between the two groups in the proportion of patients with additional analgesic drugs, postoperative wakefulness-eye opening time or 15-item quality of recovery (QoR-15) scale ( χ2=0.32, t=1.32, 1.15, P>0.05); The observation group had lower VAS scores at 30min (T1), 4 h (T2), 8 h (T3) and 12 h (T4) after surgery ( t=4.82, 6.53, 14.01, 12.87, P<0.05); At T1, T2, T3 and T4, peripheral helper T cells (Th) 1 and Th1/Th2 in observation group were higher, while Th2 was lower ( t=3.98, 4.62, 4.12, 8.52, 3.81, 9.47, 13.98, 9.53, 4.44, 4.50, 4.31, 5.45, all P<0.05); The observation group had lower tumor necrosis factor -α (TNF-α), interleukin-6 (IL-6) at T1, T2, T3 and T4, while higher IL-2 ( t=2.46, 2.99, 2.29, 3.05, 2.85, 3.64, 4.70, 2.51, 3.17, 3.74, 3.24, 2.79, all P<0.05); The incidence of adverse reactions between the two groups showed no significant difference ( χ2=2.31, P>0.05) . Conclusion:Dexmedetomidine combined with esketamine analgesia regimen can significantly improve the analgesic effect after radical mastectomy, reduce postoperative inflammatory response, and effectively protect postoperative immune function of patients, with certain safety.

Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion (I/R) in rats and the role of PI3K/Akt signaling pathway. MethodsOne hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups:Ⅰ sham operation group (group S, n =6), ⅡI/R group ( n = 30), Ⅲ propofol group (group P, n = 30), Ⅳ propofol + LY294002 group (group P+ LY, n =18), and Ⅴ propofol + dimethylsulfoxide group (group P+ DMSO, n = 18). Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg + LY294002 (a specific PI3K inhibitor) 1.5 mg/kg, and propofol 12 mg/kg + DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion (T1-5) in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt (t-Akt) and phosphorylated Akt (p-Akt) expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . ResultsCompared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ (P ＜ 0.05). Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ ( P ＜ 0.05). Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ ( P ＜ 0.05). The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. ConclusionPropofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway.