ABSTRACT
Objective To determine the median effective plasma concentration (Cp50) of remifentanil inhibiting cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Methods Twenty-two female patients scheduled for elective laparoscopic gynaecological surgery under general anesthesia, aged20-60 years, with a BMI 18-30 kg/m2, falling into ASA physical statusⅠ orⅡ, were enrolled in this study.Anesthesia was induced with propofol and remifentanil target-controlled infusion and iv injection of rocuronium 0.6 mg/kg.The target plasma concentration (Cp) of remifentanil and propofol were set at 5 ng/ml and 4μg/ml respectively.3 minutes after endotracheal intubation, the Cp of remifentanil was adjusted.The target Cp was set at 6 ng/ml in the first patient.CO2 pneumoperitoneum was performed after the target effect-site concentration and Cp were balanced.Each time Cp increased/decreased by 20％in the next patient depending on whether or not the cardiovascular response to CO2 pneumoperitoneum occurred.The positive cardiovascular response was defined as HR and/or MAP increasing by 20％ within 3 minutes after CO2 pneumoperitoneum.The Cp50 and 95％ confidence interval (CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus when combined with propofol in patients undergoing laparoscopic gynaecological surgery were calculated.Results The Cp50 (95％ CI) of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 (4.14-5.08) ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.Conclusion The Cp50 of remifentanil required to inhibit cardiovascular response to CO2 pneumoperitoneum stimulus was 4.58 ng/ml when combined with propofol in patients undergoing laparoscopic gynaecological surgery.
ABSTRACT
AIM: To investigate the mechanism of the AP-1 signal transduction pathway inhibited by JIP in nasopharyngeal carcinoma cells. METHODS: AP-1 activity was triggered by Dox-induced LMP1 expression in Tet-on-LMP1-HNE 2 cells (L7). The retention of phospho-JNK in the cytoplasm caused by JIP was examined with immunofluroscence assay. RESULTS: 24 h after transfection of L7 cells with the JIP expression plasmid, the translocation of activated JNK was inhibited, which resulted in the retention of phospho-JNK in the cytoplasm and down-regulation of the AP-1 activity. CONCLUSION: JIP down-regulates the activity of AP-1 through the inhibition of the translocation of JNK.