Objective To explore the feasibility and safety of dexmedetomidine sedation in interventional neuroradiology operations.Methods Eighty-five cases ASA grade Ⅱ-Ⅲ grade patients undergoing cerebral angiography according to age divided into two groups:old group(more than 60 years old,35 cases) and young group (18-59 years old,50 cases).The loading dose of dexmedetomidine were dexmedetomidine 0.5 μ g/kg in old group and 1.0 μ g/kg in young group,respectively.The loading dose was administered for 10 min followed by continuous infusion dexmedetomidine 0.5 μ g/ (kg· h).Blood pressure,heart rate (HR),peripheral oxygen saturation (SpO2) and respiratory rate (RR),Ramsay score and bispectral index(BIS) were monitored and recorded during the study.Results The BIS,Ramsay score after administration 10,15,30,45 min in two groups was significantly longer than that before administration [old group:84 ±22,83 ±22,85 ± 15,75 ±23 vs.94 ±5; (2.0 ±0.4),(2.3 ±0.6),(2.8 ±0.7),(3.0 ±0.7)scores vs.(1.7 ± 0.5) scores; young group:91 ± 8,89 ± 11,86 ± 12,81 ± 13 vs.96 ± 2; (1.9 ± 0.6),(2.3 ±0.7),(2.7 ± 0.9),(3.0 ± 0.9) scores vs.(1.6 ± 0.5) scores,P ＜ 0.05].The systolic blood pressure,diastolic blood pressure,mean arterial pressure (MAP) after administration 10,15,30,45 min in two groups was significantly longer than that before administration [old group:(152 ± 23),(144 ± 23),(140 ± 21),(135 ±21) mm Hg(1 mm Hg =0.133 kPa) vs.(165 ± 25) mm Hg; (87 ± 11),(83 ± 11),(78 ± 8),(75 ± 8) mm Hg vs.(89± 13)mm Hg;(106±14),(100±13),(99±12),(95±12)mm Hg vs.(113±16)mm Hg;young group:(131 ± 24),(127 ± 23),(124 ± 25),(124 ± 26) mm Hg vs.(142 ± 23) mm Hg; (81 ± 13),(79±13),(77±13),(76±13)mmHgvs.(86± 14) mmHg;(97±16),(94±16),(91±19),(92±20) mm Hg vs.(104 ± 19) mm Hg,P ＜0.05],but the decreases in blood pressure were ＜20％ from baseline.The HR,RR and SpO2 was no significant difference (P ＞ 0.05).Conclusions Continuous infusion of dexmedetomidine sedation during cerebral angiography has little effect on hemodynamics,no significant respiratory depression,is safe and effective.

OBJECTIVETo investigate the effects of Panax notoginseng saponins (PNS) on the proliferation, apoptosis and cell cycle of K562 cells and explore the molecular mechanisms underlying these effects.

METHODSPNS-induced growth inhibition of K562 cells was detected by MTT assay; the cell apoptosis was evaluated by AO/EB staining and Annexin V-FITC/ PI staining; flow cytometry was used to detect cell cycle changes in the treated cells. The mRNA expressions of the molecules in mTOR signaling pathway were examined by RT-PCR, and the cellular expressions of cleaved caspeas-3, cyclin D1 and major proteins in mTOR signaling pathway were detected using Western blotting.

RESULTSMTT assay showed that treatment with 100-800 µg/mL PNS significantly inhibited the proliferation, promoted the cell apoptosis, and caused cell cycle arrest in G0/G1 phase in K562 cells. Western blotting revealed increased protein expression of cleaved caspase-3 and decreased expression of cyclin D1 in PNS-treated cells, in which the proteins expressions of mTOR, p-mTOR, p-p70S6K and p-4E-BP 1 and the mRNA expression of mTOR were all decreased.

CONCLUSIONPNS can inhibit the proliferation, induce apoptosis and cause cell cycle arrest in K562 cells possibly by up-regulating cleaved caspase 3 and down-regulating cyclin D1 and mTOR signaling pathway.

Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Cycle ; drug effects ; Cell Cycle Checkpoints ; Cell Proliferation ; drug effects ; Cyclin D1 ; metabolism ; Humans ; K562 Cells ; drug effects ; Panax notoginseng ; chemistry ; Saponins ; chemistry ; Signal Transduction ; TOR Serine-Threonine Kinases ; metabolism ; Up-Regulation