ObjectiveTo explore sedation effect of dexmedetomidine alone and its effects on respiration and circulation of complications in transtracheal endoscopic interventional therapy. MethodsFrom April 2012 to May 2014, 60 adult patients who plan to undergo transtracheal endoscopic interventional therapy were recruited in the study. The patients were divided into a midazolam combined with fenanyl citrate intravenous injection group (MF group), and a dexmedetomidine target controlled infusion group (Y group) using the method of random number table, with 30 cases in each group. All patients were given 2% lidocaine 15 mL by ultrasonic atomizing inhalation for local surface anaesthesia preoperatively, and then the patients in MF group received midazolam and fentanyl citrate by slow intravenous injection, the patients in Y group received dexmedetomidine 0.5 g intravenous injection and persistant infusion of dexmedetomidinein dosage of 0.2 μg/h. The basic Ramsay sedation score (T0) was recorded, then the Ramsay sedation scoring was conducted when the bronchoscope entering into the pharyngeal cavity (T1), into the glottis (T2), and into the bronchial (T3), respectively. ResultsThere were no significant differences in restlessness, hypotension, hypertension, or tachycardia incidence rate between two groups (P>0.05). The differences in Ramsay score between two groups was not significant at T0 or T1 time point (P>0.05), but was significant at T2 and T3 time point (P<0.05). Compared with MF group, the incidence of respiratory depression and hypoxemia was significantly lower, and the recovery time was significantly shorter in Y group (P<0.05). All patients in Y group woke up immediately by simple call. While in MF group, 23 patients needed intravenous flumazenil to promote awakening. ConclusionDexmedetomidine alone can provide effective sedation in transtracheal endoscopic interventional therapy with good effect, high safety, and more convenient awakening.
ObjectiveTo investigate the role of sonic hedgehog (Shh) signal transduction pathway in the expression of vascular endothelial growth factor (VEGF) under hypoxia in cultured human retinal pigment epithelial (hRPE) cells. MethodsARPE-19 were cultured and divided into normal ARPE-19 (Cont) and hypoxia group (100 μmol/L CoCl2 Cobalt Chloride +ARPE-19); hypoxia group was further divided into CoCl2 group, cyclopamine group (CYA) and dimethyl sulfoxide (DMSO) group. 20μmol/L cyclopamine was added to the CYA group 1 hour before hypoxia, 1‰DMSO was added into DMSO group at the same time. The hRPE cells were cultured under hypoxia for 4, 8, 12, 24 hours. The expression of Shh and VEGF were determined by Real-time fluorescent quantitate PCR (RT-PCR). The amount of VEGF in the hRPE-conditioned supernatant was measured using enzyme linked immunosorbent assay (ELISA) at 4, 8, 12, 24 hours, respectively. ResultsRT-PCR tests showed that the level of Shh and VEGF of hRPE was time dependently increased (Shh: F=45.260, P=0.001; VEGF: F=264.938, P=0.001). The level of Shh and VEGF of hRPE in the group treated with cyclopamine was decreased (P < 0.01). ELISA tests showed that the amount of VEGF in hRPE supernatant was significantly increased in time-dependent manner (F=3 156.676, P=0.001), and it was down-regulated by cyclopamine under hypoxia (P < 0.01). ConclusionShh signal transduction pathway could play a role in the VEGF expression induced by hypoxia in hRPE cells.