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Objective To investigate the correlation between posterior neck pain and lumbar epidural pressure (LEP)during percutaneous endoscopic lumbar discectomy (PELD).Methods A prospective study was performed on 86 patients undergoing PELD,46 males,40 females,aged 1 9-71 years,with ASA physical status of Ⅰ or Ⅱ.Each patient received lumbar epidural anesthesia.Lum-bar epidural pressure (LEP)was monitored continuously through a lumbar epidural catheter which was connected to a pressure transducer.LEP before the operation (LEPbase ),LEP at the time of pos-terior neck pain (LEPpain )and maximal LEP (LEPmax )were recorded.Results Thirty patients (34.9%)complained of posterior neck pain during the procedure.The lowest LEPmax was 31.0 mm Hg,and the highest LEPmax was 77.0 mm Hg.The LEPmax in patients with neck pain [(60.6± 8.8)mm Hg]was significantly higher than LEPmax in patients without neck pain [(50.7 ± 9.5 ) mm Hg](P <0.01 ).Patients with higher LEPmax had higher probabilities of having posterior neck pain (P <0.01).Conclusion Patients with higher LEPmax had higher probabilities of having posterior neck pain.
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AIM: To explore the influence of different concentration midazolam on the macroscopic voltage gated potassium currents and to discuss the relationship between potassium currents and inhibitory effect of clinical relevant concentration midazolam on sympathetic nervous system. METHODS: Superior sympathetic ganglion neurons were dissociated enzymatically from 7 to10 day old rat. Experiments were performed about 5 h after plating at room temperature (20- 24 ℃ ). Appropriate solution was chosen to separate the K + current from the other transmembrane currents. 1 ?mol?L -1 TTX was applied to the extracelluar solution to block the Na + current. Midazolam was also resolved in extracelluar solution to get various concentration ( 0.1 , 0.3 ,3,10,50,100 ?mol?L -1 ). Currents were recorded with the patch clamp technique in whole cell configuration using glass electrodes with a tip resistance of 2- 4 M . Potassium currents were evoked by test pulse from -100 mV to +30 mV with holding potential -80mV. Data were analyzed using Clampfit 6.0 and Oringih 5.0 software. Whole cell current records were corrected for leakage and capacitance by using the P/5 protocol. RESULTS: Midazolam dose dependently inhibited the whole cell potassium currents. Clinical relevant concentration midazolam ( 0.3 ?mol?L -1 ) only reduced the peak currents by 3.89 %(P= 0.88 ). The concentration required to produce 50% current inhibition(IC 50 ) was 76.065 ?mol?L -1 . CONCLUSION: Midazolam inhibits the whole cell potassium current significantly and dose dependently, but clinical relevant concentration midazolam has minor effect on the potassium currents, indicating that the inhibitory effect of midazolam on potassium current is not related to the suppression of activity of sympathetic system.
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AIM: To study the interactions of propofol and midazolam on the whole cell sodium channel currents in rat sympathetic ganglion neurons. METHODS: Whole cell patch clamp recordings were made from enzymatically isolated rat (7- 10 d ) superior cervical sympathetic ganglion neurons. Isobolographic analysis was applied to evaluate the potency of combinations of propofol and midazolam on Na + channel currents. RESULTS: Under V h= 80 mV and V t= 0 mV . Propofol and midazolam dose dependently blocked Na + currents with a mean drug concentration required to produce 50% current inhibition (IC 50 ): 33.12 ?mol?L -1 and 18.35 ?mol?L -1 ; clinically relevant concentrations of propofol and midazolam reduced Na + peak currents by 27.66 % (P
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Aim The effects of diazepam on the whole cell sodium currents in rat sympathetic ganglion neurons were studied to investigate the mechanisms by diazepam mediates hypotension. Methods Whole cell patch clamp recordings were performed on enzymatically isolated rat superior cervical sympathetic ganglion neurons. Results Diazepam dose dependently blocked the whole cell sodium currents. Under a V t of 0 mV and a V h of 80 mV 0.3 ?mol?L -1 diazepam reduced sodium peak currents by 14.76 %(P
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ve To investigate the effects of clinical relevant concentrations of midazolam on whole-cell N-type calcium currents of sympathetic ganglion neurons trying to assess the involvement of sympathetic ganglion in circulation depression produced by midazolam. Methods 7-10 d SD rats were decapitated and bilateral superior cervical ganglions were rapidly removed and kept in 4℃, oxygen saturated incubation solution. TTX 1?mol/L and nifedipine 10 ?mol/L were added to the solution to block the Na+ and L-type calcium currents. Midazolam was also added to the solution. The final concentration of midazolam were 0.1, 0.3, 3, 10, 50, 100?mol/L.The effects of different concentration of midazolam on the whole-cell N-type calcium channel currents were assessed by patch-clamp technique. Results When the holding potential (Vh) was - 80mV and stimulating votage(Vt) was between - 30mV and 10mV midazolam inhibited the whole-cell N-type calcium currents dose-dependently ( r = 0.964, P