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Objective To evaluate the effect of the combination of dexmedetomidine and sufentanil on monitoring anesthesia care during burr-hole surgery for patients with chronic subdural hematoma. Methods 96 pa-tients underwent burr-hole surgery for chronic subdural hematoma with MAC were randomly divided into two groups:Group D and Group DS (n=48 in each group). Local anesthetic block was started at least 10 min after DEX and sufentanil infusion. Ramsay sedation scale of the two groups was maintained to 3. Anesthesia onset time, hemo-dynamics, the amount of rescue midazolam or fentanyl, the time to first dose of rescue midazolam or fentanyl, the to-tal number of intraoperative patient movements, postoperative recovery time, patient and surgeon satisfaction scores, and the adverse events were recorded. Results Compared with group D, anesthesia onset time was significantly less in group DS (13.68 ± 3.13 vs. 11.82 ± 2.43 min, P=0.002). More patients in group D required rescue midazol-am to achieve RSS=3 compared with group DS (31.25%15/48 vs. 12.50%6/48, P=0.023). Compared with group D, significantly fewer patients in group DS required rescue fentanyl to relieve pain (10.42%5/48 vs. 27.08%13/48, P = 0.036). Additionally, the total dose of rescue fentanyl in group DS was significantly higher (89.48 ± 23.27 vs. 125.28 ± 33.52μg, P=0.000), and the time to first dose of rescue fentanyl was longer than group D(18.34 ± 4.45 vs. 14.34 ± 3.63 min, P=0.000). The total number of patient movements during the burr-hole surgery was higher in group D than group DS (35.42%17/48 vs. 16.67%8/48, P=0.036). The time to recovery for discharge from the PA-CU (time to an Aldrete score ≥ 9) was significantly shorter in group DS compared with group D (17.54 ± 5.92 vs. 12.57 ± 5.28 min, P=0.000). Results from the patient and surgeon satisfaction scores showed significant differenc-es favoring group DS (P<0.05). More patients in group D showed higher levels of the overall incidence of bradycar-dia (37.50% 18/48 vs. 18.75% 9/48, P = 0.041) and hypotension(37.50%18/48 vs. 14.58%79/48, P=0.011)com-pared with group DS. Conclusions Compared with DEX alone, DEX-sufentanil associated with fewer number of in-traoperative patient movements, less amount of rescue scheme, could be safely and efficiently used for MAC during burr-hole surgery for patients with chronic subdural hematoma.
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Objective To observe the effect of combination of dexmedetomidine and sufentanil on postoperative analgesia for the highly nicotine dependent patients undergoing esophagectomy. Methods Ninety highly nicotine dependent patients undergoing esophagectomy were randomly allocated into three groups (n = 30 each): low-dose sufentanil group (Group S1), high-dose sufentanil (Group S2), dexmedetomidine and sufentanil group (Group DS). All patients of three groups received postoperative PCIA with following setting: 2 mL/h;bolus: 2 mL; lock time: 5 min; 4 hours limited: 40 mL. The scores of VAS and Ramsay, effective presses/total presses of PCIA, the consumption of sufentanil during 72 h after operation, side effects and the satisfaction degree of patients were recorded. Results Compared with those of group S2, the scores of VAS (both at rest and movement) decreased significantly in group DS from 1 h to 8 h (P<0.05). Compared with those of group S1, the scores of VAS (both at rest and movement) decreased significantly in group S2 and DS from 1 h to 72 h (P<0.05). Compared with that in group S1 and S2, the consumption of sufentanil during 72 h after operation decreased significantly in group DS (P < 0.05). Compared with those in group DS, The numbers of nausea and vomiting were significant decreased in group S1 and S2(P < 0.05). Compared with those in group S1, the remedial cases were significantly decreased in group S2 and group DS (P < 0.05). Conclusion The effect of combination of dexmedetomidine and sufentanil is superior to that of sufentanil in terms of postoperative analgesia in highly nicotine dependent male patients undergoing esophagectomy.
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Aim To pick out the siRNA which could most effectively inhibit the expression of TLR4 in microglial cells and to detect the cytotoxicity of the transfection complex.Methods Five siRNAs were chemicaly synthesized:four of them were used to inhibit TLR4 expression in microglial cells,the rest was fluorescence-labeled mismatch siRNA as a nagative control.They were all transfected into microglial cells,respectively.TLR4 mRNA was detected 24 h after transfection by RT-PCR and its protein expression wasobserved by Western blot 48 h later.The cytotoxicity of complex was detected using MTT.Results ① The transfection rate was high enough in microglial cells with siRNA(40 pmol)and LipofectamineTM 2000(1 μl).② The TLR4 siRNA pool reduced TLR4 mRNA by 85%(siRNA_(439)),73%(siRNA_(312)),67%(siRNA_(1495))and 33%(siRNA_(2062))respectively compared with mismatch siRNA-treated group 24 h after transfection in a microglial cell line.③ The TLR4 siRNA439 was the most effective siRNA(P<0.01).④ The cell survival rates were above 85% in the groups of Lipofectamine~(TM) 2000 1 μl compound less than 40 nmol·L~(-1) siRNA.Conclusions ① The TLR4 siRNA_(439) can inhibit TLR4 expression most effectively in microglial.② 40 nmol·L~(-1) siRNA and 1 μl Lipofectamine~(TM) 2000 have low cytotoxicity,which are suitable for transfection.
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Objective To evaluate the role of brain-derived neurotrophic factor (BDNF) in inflammatory pain in rats. Methods Sixty female SD rats weighing 150-180 g in which intrathecal (IT) catheters were successfully placed without complication were randomly divided into 5 groups (n= 12 each): group Ⅰ sham operation; group Ⅱ sham operation + IT anti-BDNF antibody; group Ⅲ inflammatory pain; group Ⅳinflammatory pain + IT control IgG and group Ⅴ inflammatory pain + IT anti-BDNF antibody. Inflammatory pain was induced by injecting complete Freund's adjuvant (CFA) into ankle joint cavity of left hindpaw, while in sham operation group equal volume of normal saline was injected instead of CFA. Anti-BDNF antibody or control IgG 15 μg/10 μl was injected IT once a day for 3 days after inflammatory pain was induced. Paw withdrawal latency to thermal stimuli (PWTL) was measured one day before and at 3, 5, 7, 10 and 14 d after inflammatory pain was induced. The rat was sacrificed on 3 rd day of IT anti-BDNF antibody or control IgG injection. The lumbar segment L4-6 of the spinal cord was removed for detection of the expression of BDNF and p-ERK1/2 by immunohistochemistory and Western blot. Results Intra-articular CFA injection significantly increased the expression of BDNF and p-ERK1/2 in the spinal cord in group Ⅲ as compared with sham-operated animals in group Ⅰ . IT antiBDNF antibody injection significantly suppressed the expression of BDNF and p-ERK1/2. PWTL was significantly shortened after intra-articular CFA injection in group Ⅲ as compared with group Ⅰ . IT anti-BDNF antibody reversed the inflammation-induced thermal hyperalgesia in group Ⅴ but IT control IgG did not. Conclusion BDNF in the spinal cord may be involved in inflammatory pain through p-ERK1/2 signal transduction pathway.
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Objective To evaluate the changes in expression of NF-κB, IL-6 and TNF-α in spinal cord in a rat model of bone cancer. Methods Seventy-two female SD rats weighing 150-180 g were randomly divided into 3 groups (n = 24 each): control group (group C);sham operation group (group S) and bone cancer pain group (group BP). Bone cancer was induced by intra-tibial inoculation of 1 × 105 Walker 256 breast cancer cells. Paw withdrawal threshold to mechanical stimulation was measured with yon Frey filaments. The expression of NF-κB p65, IL-6 and TNF-α mRNA in the spinal cord was determined by RT-PCR and the expression of NF-κB p65 by immuno-histochemistry and NF-κB p65 positive cell count was determined. Results The paw withdrawal threshold was significantly lower and the expression of NF-κB p65, NF-κB p65 mRNA, IL-6 mRNA, TNF-α mRNA and NF-κB p65 positive cell count in the spinal cord were significantly higher in group BP than in group C and S ( P ＜0.05 or 0.01 ). Conclusion Intra-tibial inoculation of Walker 256 breast cancer cells activates NF-κB in the spinal cord, leading to the increased release of IL-6 and TNF-α and mechanical hyperalgesia.