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Objective To evaluate the effect of sleep dysfunction on sedation induced by propofol in the patients undergoing radical mastectomy.Methods One hundred breast cancer patients,aged 25-60 yr,with body mass index of 19-23 kg/m2,of ASA physical status Ⅰ or Ⅱ,scheduled for elective modified radical mastectomy,were randomly divided into 2 groups according to sleep quality.The patients with global Pittsburgh Sleep Quality Index (PSQI) score ≤7 served as regular sleep quality group (Ⅰ group,n =59).The patients with global PSQI score ＞ 7 served as sleep dysfunction group (group Ⅱ,n =41).Anesthesia was induced with propofol given by target-controlled infusion (target plasma concentration of 3.5 μg/ml),and then with remifentanil 4 μg/kg and rocuronium 0.6 mg/kg after loss of consciousness.The consumption of propofol at loss of consciousness was recorded.Results Compared with group Ⅰ,the consumption of propofol at loss of consciousness was significantly decreased in group Ⅱ.Conclusion Sleep dysfunction can enhance propofol-induced sedation in the patients undergoing radical mastectomy.
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Objective To evaluate the effect of chemotherapy on sedation with propofol in breast cancer patients.Methods One hundred female patients,of ASA physical status Ⅰ or Ⅱ,aged 20-60 yr,scheduled for elective modified radical mastectomy,were divided into 2 groups (n =50 each) according to whether receiving neoadjuvant chemotherapy before operation:non-chemotherapy group (group Ⅰ) and neoadjuvant chemotherapy group (group Ⅱ).The breast cancer patients received operation directly in group Ⅰ.The breast cancer patients received neoadjuvant chemotherapy in group Ⅱ.Epirubicin 75-100 mg/m2 was injected intravenously on 1st and 2nd days,docetaxel 75 mg/m2 was injected intravenously on 3rd day,and 3 weeks were considered as 1 course of treatment.The patients received operation at 3 weeks after the end of 4 courses of treatment in group 1.Anesthesia was induced with propofol given by target-controlled infusion and the target plasma concentration of propofol was 3.5 μg/ml.The time for loss of consciousness and consumption of propofol at loss of consciousness were recorded.Results Compared with group Ⅰ,the time for loss of consciousness was significantly shortened,and the consumption of propofol at loss of consciousness and BIS value were decreased in group Ⅱ.Conclusion Chemotherapy can enhance propofol-induced sedation and promote the onset of propofol in breast cancer patients.
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Objective To investigate the effect of carbon dioxide ( CO2 ) pneumoperitoneum on the neuromuscular block of cisatracurium in patients undergoing laparoscopic operation.Methods Sixty ASA Ⅰ or Ⅱ patients,aged 35-60 yr,with body mass index of 18-24 kg/m2,scheduled for elective hysterectomy,were randomly divided into 2 groups ( n =30 each ):pneumoperitoneum group ( group P) and control group ( group C ).Each group was further divided into 2 subgroups according to the use of the antagonist of neuromuscular block ( n =15 each):no neostigmine group ( group P0 or C0 ) and neostigmine group (group P1 or C1 ).Anesthesia was induced with fentanyl,propofol and cisatracurium and maintained with target-controlled infusion of propofol and remifentanil.Tracheal intubation was performed and the patients were mechanically ventilated.Neuromuscular function was monitored by TOF-Watch SX accelerography (Organon Co.,Organon).A train of four (TOF) stimulation of the ulnar nerve was used.When T,returned to 5％ of control height after CO2 pneumoperitoneum was established,cisatracurium 0.05 mg/kg was injected intravenously in group P.When T1 returned to 25％ of control height after the end of operation,neostigmine was injected intravenously in groups P1 andC1.The clinical duration and recovery index were recorded after CO2 pneumoperitoneum was established.Arterial blood samples were obtained immediately before induction,at 30 and 60 min of pneumoperitoneum,and at the end of operation for blood gas analysis.Results The clinical duration and recovery index were significantly longer in group P0 than in group C0,and in group P1 than in group C1 ( P ＜ 0.05).Compared with group C0,the pH value was significantly decreased and PaCO2 was significantly increased at 30 and 60 min of pneumoperitoneum,and at the end of operation in group P0 ( P ＜ 0.05).Compared with group C1,the pH value was significantly decreased and PaCO2 was significantly increased at 30 and 60 min of pneumoperitoneum,and at the end of operation in group P1 ( P ＜ 0.05).Conclusion CO2 pneumoperitoneum can strengthen the neuromuscular block induced by cisatracurium and prolong the recovery time following antangonism by neostigmine administration in patients undergoing laparoscopic operation.
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Objective To investigate the effects of fentanyl and remifentanil on the viability of human adenocarcinoma cell line A549.Methods Human adenocarcinoma A549 cells cultured in logarithmic growth phase were seeded in 75 ml culture bottles or 96-well plates.After being cultured for 24 h,the cells were randomly divided into 9 groups (n =30 each):4 fentanyl groups (groups F1-4 ),4 remifentanil groups (groups RF1-4 ) and control group (group C).Groups F1-4 were exposed to fentanyl with the final concentrations of 0.5,5.0,50.0 and 500.0 ng/ml respectively.Groups RF1-4 were exposed to remifentanil with the final concentrations of 0.5,5.0,50.0 and 500.0 ng/ml respectively.The viability of the cells was determined by methyl thiazolyl tetrazolium assay after being incubated for 24,48 and 72 h.The cell cycle progression and apoptosis were determined by flow cytometry after being incubated for 24 h.Results Compared with group C,the viability of A549 cells were gradually decreased at 72 h of incubation,the proportion of the cells in S phase was gradually decreased at 24 h of incubation,and the proportion of the cells in G2/M phase and apoptotic rate were gradually increased in groups F2-4 and in groups RF2-4 ( P ＜ 0.05).Conclusion Fentanyl and remifentanil with the final concentration ≥5 ng/ml can inhibit the viability of human adenocarcinoma cell line A549 in a dose-independent manner by inducing cell apoptosis and cell cycle arrest in G2/M phase.