Objective: To examine the effects of midazolam-induced sedation on heart rate variability (HRV). Method:Fifteen ASA Ⅰ- Ⅱ adult patients,undergoing elective surgery under lumbar epidural anesthesia were randomly selected. An intravenous bolus dose of midazolam(1.5mg) was administered every 3-5 minutes until patients' sedation levels assessed by observers assessment of alertness sedation(OAA/S) scale had scores of 1. Spectral analysis of HRV was performed at different OAA/S scores and at 3min,5min and 10min following OAA/S score of 1. Result:All frequency components of HRV were significantly reduced as patients' OAA/S scores decreased,especially low frequency (LF) and total power. Midazolam decreased normalized unit power of LF from 33.5%?8.9% to 16.65?9.6% and increased normalized unit power of high frequency(HF) from 11.7%?4.2% to 20.5%?26.5%. LF/HF ratio also reduced. Conclusion:Midazolam shiftes the balance of autonomic nervous activity toward the parasympathotonic.

BACKGROUND: With the continuous development of materials science, magnesium alloy vascular stent materials have become a hot research. Because of the mechanical properties and biocompatibility of commercial magnesium alloy, it is difficult to meet the requirements of vascular stents. Therefore, effective measures to improve the sten's surface properties and comprehensive performance become the focus of research.OBJECTIVE: To study the histology and surface modification of vascular stents in rapidly solidified Mg-Zn-Y-Nd alloy.Methods: The low-zinc Mg-2Zn-0.2Y alloy with good mechanical properties and corrosion resistance was selected as the basic material, and Nd and Zn elements were added to refine the alloy stents. After the microstructure of the stent was extruded, the surface modification of the stent was completed and the comprehensive properties of the alloy were improved. The new magnesium alloy for the stent was obtained and the stent surface was modified. The metallographic microstructure, scanning electron microscopy and radiological analysis were used to study the microstructure and mechanical properties of the prepared stents. The mechanical properties of the stents were investigated by hardness and tensile tests.RESULTS AND CONCLUSION: (1) Metallographic microstructure results showed that: when Y elements were not added, the second phase of the magnesium alloy was rod-shaped, and there were a few granules embedded in the matrix. After addition of 0.5% Y elements, in the second phase of the magnesium alloy stent, the shafts were significantly reduced in number, and granules were increased in number and evenly distributed in the body. After the addition of 1% Y,the second phase number increased, a large number of dendrites were visible in the grains, and discontinuous rods existed in the second phase. After the addition of 1.5% Y, the second phase was rod-shaped, with mixture of large and local dendrites in the alloy. (2) X-ray diffraction test results: Mn-Zn-0.5Nd alloy and Mn-Zn-1.0Nd alloy contained the same phases (Mg4Zn7 and (Nd, Y) 2Zn17 phase). When the concentration of Nd increased to 1%, the new MgZn2 phase appeared in the alloy. (3) SEM & EDS test results of modified magnesium alloy showed that after magnesium alloy modification, the second phase contained Zn, Nd and Y elements, and their contents were very close. EDS analysis showed that after the addition of Zr elements, the level of Zn elements in the lamellar second phase decreased significantly, and the level of Nd and Y elements increased, indicating a more stable performance. (4) Micro-hardness test results showed that with the increasing of the content of magnesium alloy, the alloy microhardness increased. (5)Tensile test results showed that the tensile strength and yield strength of the Mg-Zn-Y-0.5Nd-Zr stent were significantly higher than those of Mg-Zn-Y-0.5Nd, Mg-Zn-Y-1.0Nd,Mg-Zn-Y-1.0Nd-Zr stents (P < 0.05); and the elongation at break of Mg-Zn-Y-0.5Nd-Zr and Mg-Zn-Y-1.0Nd-Zr stents was significantly higher than that of Mg-Zn-Y-1.0Nd and Mg-Zn-Y-0.5Nd stents (P < 0.05). To conclude, with Mg-2Zn-0.2Y as core materials, the material modification could be completed by the addition of Nd and Zn elements, and the surface modification could be implemented by extruding and refining the stent microstructure. The modified material has excellent properties.

Objective To evaluate the effect of intrathecal IL-10 gene on neuropathic pain induced by chronic constriction injury (CCI) to the sciatic nerve. Methods Sixty female SD rats weighing 230-250 g were anesthetized with pentobarfaital. Right sciatic nerve was exposed at the midthigh level and 4 ligatures were placed on the sciatic nerve with 4.0 catgut at 1mm interval. Intrathecal catheter (PE-10 tubing) were inserted at L5,6 interspace and correct placement was confirmed by outflow of CSF. The animals were randomized into 5 groups ( n = 12): group Ⅰ sham operation; group Ⅱ CCI; group Ⅲ,Ⅳ and Ⅴ received intrathecal (IT) normal saline (NS) (Ⅲ) or pcDNA 3.1 (Ⅳ) or pcDNA 3.1-IL-10 (Ⅴ) 3 days after CCI when the animals developed thermal hyperalgesia. Threshold to noxious thermal stimuli was measured before CCI (baseline), before and 2, 4, 7, 10 and 14 days after IT injection. CSF was collected on 1, 3, 7 and 10 days after IT injection for determination of CSF IL-10 concentration. Six animals were killed on 3rd and 14th days after IT injection respectively in each group and the sciatic nerve, lumbar segment of spinal cord ( L3-6) and hippocampus were isolated and blood was collected for determination of IL-10 mRNA expression (by RT-PCR) (on 3rd day after IT) and TNF-? content (on 14th day after IT) .Results Paw removal latencies were significantly longer 2-14 days after IT injection in group Ⅴ(CCI + pcDNA 3.1-IL-10) than in group Ⅲ (CCI + NS) and Ⅳ (CCI + pcDNA 3.1). The IL-10 mRNA expression in sciatic nerve, lumbar segment of spinal cord and hippocampus was significantly higher 3 days after IT injection while their TNF-? contents were significantly lower 14 days after IT injection in group Ⅴ than in the other 4 groups. The CNS IL-10 concentration on day 1-7 after IT injection was significantly higher in group Ⅴ than in the other 4 groups. Conclusion Intrathecal IL-10 gene injection can ease pain induced by CCI of the sciatic nerve through inhibition of inflammatory response.

Objective: To analyse correlation of bispectral index,spectral edge frequency of electroencephalogram with midazolam-induced sedation. Method: 30ASA grade Ⅰ-Ⅱ adult patients, undergoing elective surgery under regional anesthesia were randomly devided into three groups according to intravenous bolus doses of midazolam,i, e. group Ⅰ:0.05mg?kg~(-1),group Ⅱ:0.1mg?kg~(-1),group Ⅲ:0.2mg?kg~(-1). After an intravenous bolus dose of mida zolam was administered,both bispectral index (BIS), 95% spectral edge freguency (SEF) of electroencephalogram were monitored and their correlation with midazolam induced sedation was analysed. Result: Both BIS and 95% SEF-correlated with midazolam-induced sedation significantly (r= 0.86,0.73, P

Objective: To explore the effects of desflurane on systemic and hepatic hemodynamics and oxygen delivery to the liver. Method: 11 healthy mongrel dogs were anesthetized with 0.5 and 1.0 MAC desflurane respectively. The changes of systemic, pulmonary and hepatic hemodynamics,systemic oxgen delivery and consumption,oxygen delivery to the liver were measured continuously. Blood flow of hepatic artery and portal vein was monitored with electromagnetic flowmeter. Result: During inhalation of 0.5 MAC desflurane,HR.MAP.SVR,portal vein and total hepatic oxygen delivery decreased significantly(P

Objective To investigate the effects of midazolam on the delayed rectifier outward potassium channel current (Ik) using the whole-cell patch clamp technique. Methods Pyramidal neurons were isolated acutely from 5-15 d SD rat hippocampus. We measured amplitudes of the delayed outward rectifier potassium currents by activating depolarizing pulse from - 50mV to 30mV. Different concentrations of midazolam were added and potassium channel currents were measured. Results Delayed outward rectifier potassium channel currents were inhibited by midazolam in a dose-dependent manner. EC50 was (8.31 ?2.78) ? 10-8 mol/L and Hill constant was 0.90? 0.16.Conclusions Our results suggest that block of the outward rectifier potassium channel current by midazolam may contribute to the mechanism of midazolam anesthesia action.

Objective To study the effects of propofol on enhancement of persistent sodium currents in isolated rat hippocampal CA1 pyramidal neurons induced by ischemia. Methods Whole-cell patch clamp recordings were made from enzymatically isolated SD rat hippocampal CA1 pyramidal neurons. Ischemia was induced by anoxia and glucose deprivation. Results Both propofol 10 umol.L-1 and 100umol . L-1 significantly inhibited the enhancement of persistent sodium currents induced by ischemia and the effect of propofol 100 umol. L-1 was significantly greater than that of propofol 10umol.L-1 . Propofol 1 umol.L-1 didn't have any significant eflect on the enhanced persistent sodium currents induced by ischemia.Conclusion Propofol can inhibit the enhancement of persistent sodium currents induced by ischemia. It may explain the cerebral protective effect of propofol.

Objective Potassium channel is essential for excitability of neurons and is involved in the regulation of information transmission. The purpose of this study was to investigate the effect of propofol on the voltage-gated potassium channels in rat hippocampal pyramidal neurons. Methods SD rats of 5-15 days old were decapitated and brain was immediately removed. Hippocampal pyramidal neurons were freshly isolated. Whole-cell patch clamp recordings were made. Voltage-dependent sodium and calcium currents were inhibited by TTX 1?mol?L-1 and CdCl2 400 ?mol?L-1 added to the perfusate. The effects of propofol on transient outward potassium currents and delayed rectifier potassium currents were studied and also the kinetics of channels. Results All the channels studied were reversibly inhibited by propofol in a dose-dependent manner. EC50 of propofol on transient outward potassium channels and delayed rectifier potassium channels were (71?18) ?mol?L-1 and (37?18) ?mol?L-1 respectively. The maximum inhibition rates were 52%?3% and 32%?5% .Conclusion Propofol reversibly inhibits potassium currents in a does-dependent manner. It is inferred that propofol affects the excitability of hippocampal neurons.

Objective To evaluate the effects of propofol and thiopontal on calcium and potassium channels in rat ventricular myocytes and to elucidate the underlying mechanisms of their inhibitory effect on myocardium. Methods Freshly isolated ventricular myocytes were prepared from hearts of rats by trypsin. The effects of propofol and thiopental on L-type calcium current(Ica) and delayed rectifier potassium current(IK)were compared using whole-cell patch clump technique. Results Propofol and thiopontal produced a concentration-dependent inhibition of Ica. Peak concentration of propofol(50 ?mol?L~(-1)) and thiopental(100 ?mol?L~(-1)) during induction of anesthesia decreased Ica by 28% and 46% and shifted the steady-state inactivation curve to more negative voltage, but had no effect on the steady-state activation curve. Propofol and thiopental also decreased IK in a concentration-dependent manner, but the effects of both anesthetics on IK were smaller compared with their effects on Ica. Conclusion The findings of this study suggest that the negative inotropic of propofol and thiopental are, at least in part, related to decrease in Ca~(2+) trans-sarcolemmal current by accelerating L-type calcium channel inactivation. Both anesthetics decrease delayed rectifier potassium current, thus partially antagonizing the effect of decreased calcium current.

Objective To investigate the inhibitory effects of fentanyl on GABAA receptors in hippocampal pyramidal neurons of rat.Methods Pyramidal neurons were acutely isolated from 3-10 day old SD rats of either sex by enzymatic-mechanic method. GABAA receptor mediated currents ( IGABA) were recorded using voltage clamped whole cell patch clamp technique in gap-free mode at the holding potential (VH) of - 50 mV. Current-voltage relationship of IGABA was obtained in ramp protocol ranging from + 30 mV to - 110 mV and lasting for 1 600 ms. Data were collected by using a system consisting of Axopatch 200B patch-clamp amplifier, Pentium Ⅲ computer and Digidata 1200 interface. All experiments were performed at room temperature (22-25℃). Five to twelve neurons were used for each fentanyl concentration. The effects of fentanyl from 1.0 ? 10-5 ?mol?L-1 to 10. 0 ?mol?L-1 were evaluated by the inhibition rate of the peak amplitude of IGABA, the desensitization time constant (?des) of IGABA and the reversal potential (Ecl- ) of IGABA. A ?-opioid receptor selective antagonist CTAP 1 ?mol?L-1 was applied and its effects on fentanyl were recorded. Results (1) GAB A 1-1 000 ?mol?L-1 induced inward currents (IGABA) dose-dependently with an EC50 of 23.73 ?mol?L-1.IGABA induced by GABA 30 ?mol?L-1 was blocked by bicuculline 1 ?mol?L-1. (2) Fentanyl depressed IGABA dose-dependently with EC50 of 0.011 ?mol?L-1 and shortened the rdes of IGABA.(3) The inhibitory effects of fentanyl on IGABA were antagonized by CTAP. (4) Fentanyl 0.01 ?mol?L-1 and CTAP did not influence the reversal potential of IGABA (Ecl- -3.0 mV) .Conclusion Fentanyl inhibits the function of GABAA receptors through ?-opioid receptors in hippocampal pyramidal neurons. Hippocampus may play a role in the neuroexcitatory effects of opioids.