Objective To investigate the effects of inhalation of isoflurane (Iso) on pulmonary and systemic inflammatory response through the changes in the plasma and pulmonary levels of IL-1β and IL-10 in rats. Methods Thirty-two adult male Wistar rats were randomly divided into 4 groups (n=8 each): group control (group C), group Iso-4 h, group Iso-8 h and group R. Group C inhaled air only. Group Iso-4 h and Iso-8 h inhaled in 40% O2 + 1.5% Iso for 4 and 8 h respectively. Group R inhaled 40% O2 + 1.5% Iso for 8 h and then withdrew and only inhaled 40 % O2 for 2 h. Blood samples were taken from femoral artery for measurement of plasma concentrations of IL-1β and IL-10 by ELISA. Then the rots were sacrificed to collect bronchoalveolar lavage fluid (BALF) for measurement of IL-1β and IL-10 concentrations. The right lung tissues were obtained for determination of the expression of IL-1β mRNA and IL-10 mRNA by RT-PCR. Results The BALF concentration of IL-1β and IL-1β mRNA expression in lung tissues were significantly higher in group Iso-4 h, and the concentrations of plasma and BALF IL-1β and IL-10, and the expression of IL-1β mRNA and IL-10 mRNA in lung tissues were significantly higher in group Iso-8 h than in group C (P<0.05), but there were no significant differences in the concentrations of plasma and BALF IL-1β and IL-10 and expression of IL-1β mRNA and IL-10 mRNA in lung tissues between group R and group C (P>0.05). The plasma and BALF IL-10 concentrations and IL-10 mRNA expression in lung tissues were significantly higher in group Iso-8 h than in group Iso-4 h (P<0.05). The concentrations of plasma and BALF IL-1β and IL-10 and expression of IL-1β mRNA and IL-10 mRNA in lung tissues were significantly lower in group R than in group Iso-8 h (P<0.05). Conclusion Isollurane inhalation can induce transient pulmonary and systemic inflammatory response in rats.

0.05).Conclusions Combined spinal and epidural anesthesia combined with target controlled infusion of midazolam has slight side effects and serum cortisol changes,suitable for gynecological operations.

Objective:To examine the effects of different concentrations of Isoflurane on the level of surfactant protein A(SP-A) and the expression of SP-A mRNA in the lung of rats.Methods: Thirty-two male Wistar rats were randomly divided into 4 groups: control group received 40%(volume fraction) O_2 inhalation(40% O_2,n=8);0.7% isoflurane group(n=8),1.5% isoflurane group(n=8).They and 2.0% isoflurane group(n=8).They were treated with 40%O_2 with 0.7%,1.5% and 2.0% isoflurane respectively.In each group,the rats inhaled experimental gas for 8 hours,and then were put to death immediately.Morphological changes of type Ⅱ pneumocytes were observed by transmission electron microscopy.Surfactant protein content in broncho-alveolar lavage fluid(BALF) was measured with Western Blotting.The level of intracellular SP-A was examined with immunohistochemistry(IHC).To assess the relative levels of SP-A mRNA in lung tissue,reverse transcriptase-polymerase chain reaction(RT-PCR) was used with the co-amplification of the "housekeeping" gene GAPDH as internal control.Results: Morphological changes of type Ⅱ pneumocytes were distinct in 1.5% isoflurane and 2.0% isoflurane groups.Isoflurane,after three doses,significantly reduced the SP-A content in BALF.Control group,(437 112)?25 654;0.7%Isoflurane group,355 789?28 116;1.5%Isoflurane group,238 554?31 531;(2.0%) Isoflurane group,223 632?25 710(P

Objective To investigate the effects of inhalation of different concentrations of sevoflurane on pulmonary inflammatory response in rats. Methods One hundred and twenty adult Wistar rats of both sexes weighing 200-250 g were randomly divided into 4 groups: Ⅰ control group breathing room air (group C, n = 12);Ⅱ oxygen group breathing 40% O2(group O, n = 36);Ⅲ and Ⅳ sevoflurane groups breathing 1.5% and 3.0% sevoflurane in 40% O2 respectively (group S1, S2, n = 36). Group Ⅱ was further divided into 3 subgroups according to the duration of 40% O2 inhalation 4 h, 8 h and 10 h. Group Ⅲ and Ⅳ were further divided into 3 subgroups ( n = 12 each) breathing sevoflurane for 4 h, 8 h and 8 h followed by 2 h O2 (40%) inhalation. The animals were sacrificed at the end of O2 or/and sevoflurane inhalation. Broncho-alveolar lavage was performed in 6 animals in each subgroup. The TNF-α concentration in broncho-alveolar lavage fluid was determined. The TNF-α mRNA expression and MPO activity in the lung tissue were measured in the other 6 animals in each subgroup. Results Inhalation of 1.5% or 3.0% sevoflurane for 4 or 8 h did not induce inflammatory response in the lung as compared with animals breathing room air or 40% O2 . Conclusion Exposure to sevoflurane does not induce pulmonary inflammatory response in rats breathing spontaneously.

Objective To determine the pharmacokinetics and pharmacodynamics of chloroprocaine with or without epinephrine for epidural blockade. Methods Twenty ASA physical status Ⅰ or Ⅱ patients of both sexes aged 37-55 yrs weighing 45-80 kg undergoing elective lower abdominal surgery were randomly divided into 2 groups (n = 10 each): group C chloroprocaine without epinephrine and group CE chloroprocaine with epinephrine. The epidural catheter was inserted into epidural space at T12-L4 and advanced toward head for about 4 cm. After correct epidural placement was confirmed,3% chloroprocaine 6 mg?kg-1 with or without 1:200 000 epinephrine was injected into epidural space over 2 min. Onset time of analgesia , motor blockade and degree of motor blockade at 20 min after epidural injection (Bromage scale 0 = no motor block, 3 = unable to flex hip, knee and ankle) were recorded. Blood samples were taken from radial artery before and at 3, 6, 9, 11, 13, 15, 17, 20, 30, 45, 60, 90 min after epidural injection for determination of plasma chloroprocaine concentration by HPLC. Results The two groups were comparable with respect to demographic data. There were no significant differences in the pharmokinetics and pharmacodynamics of chloroprocaine between the two groups. The Cmax was (0.491?0.47) mg?L-1 and (0.32?0.22) mg?L-1; The Tmax was (8?3) min and (9?4) min; the AUC was (10?6) ?g?min?ml-1 and (7?4) ?g?min?ml-1;the K was 0.32?0.21 min-1 and 0.36?0.32 min-1 in group C and CE respectively. Conclusion Epinephrine 1:200 000 does not affect the pharmacokinetics and pharmacodynamics of 3 % chloroprocaine for epidural block.

Objective To investigate the effects of 1% ropivacaine injected epineurally or intraneurally on the recovery of sciatic nerve from acute injury in rats. Methods Seventy-two healthy male Wistar rats weighing 220-250 g were xandomly assigned into 4 groups ( n = 18 each): group Ⅰ epineural injection of normal saline(NS)(group C1); group Ⅱ intraneural injection of NS (group C2); group Ⅲ epineural injection of 1% ropivacaine (group Epi-R) and group Ⅳ intraneural injection of 1% ropivacaine (group Intra-R). The animals were anesthetized with intraperitoneal 3% pentobarbital 60 mg/kg. The sciatic nerve was exposed and crushed with blood vessel clamp for 2 min. NS or 1% ropivacaine 0.2 ml was injected epineurally or intraneurally after release of the clamp.Sciatic nerve function was measured and sciatic nerve function index (SFI) was calculated at day 1, 3, 7, 14, 21and 28 after operation. Six animals in each group were anesthetized on the 14th and 28th day after operation and the nerve conduction velocity (NCV) of the sciatic nerve was measured. The sciatic nerve was then removed for histologic examination. Results There was no significant difference in SFI and NCV at all time points among group C1 , C2 and Epi-R. SFI was almost normal on the 28th day after operation in the 3 groups. The NCV was significantly slower at day 14 and 28 after operation in intra-R group than in the other 3 groups. Conclusion Intra-neural injection of ropivacaine can significantly delay the recovery of sciatic nerve from acute injury.

Objective To evaluate the performance of the target controlled infusion(TCI) system with midazolam during combined spinal and epidural anesthesia. Methods Twenty female patients scheduled for selective lower abdominal or pelvic surgery under combined spinal and epidural anesthesia were enrolled in this study. They use combined spinal and epidural anesthesia with target controlled infusion of midazolam sedation. Midazolam plasma concentration was set at 100ng/ml. Blood pressure,heart rate, pulse oxygen saturation were monitored during anesthesia and operation. We use BIS as a pharmacodynamic value of midazolam sedation. Blood samples were taken from radial arterial for analysis of plasma midazolam concentration during infusion. Midazolam plasma concentration were tested by high performance liquid chromatography. Results MDPE of target controlled infusion with midazolam with Burher parameters was 38.7%, MDAPE was 38.7%,and wobble is 24.9% in Chinese female patients. Conclusions Burher parameters of midazolam target controlled infusion system should be correct, then can be used for our country female patients conscious sedation accurately.

Objective To investigate the changes in oxygenation and intrapulmonary shunt duringprolonged one-lung ventilation (OLV) and compare the effects of four different anesthetic techniques. MethodsForty ASAⅠ -Ⅱ patients (27 male, 13 female) aged 36-74 yr undergoing prolonged OLV during elective thoracicsurgery were randomly allocated to one of four groups: (1) isoflurane (GI, n = 10); (2) isoflurane + epidural(GIE, n =10); (3) propofol (GP, n = 10); (4) propofol + epidural (GPE, n = 10). Radial artery wascannulated and Swan-Ganz catheter was placed via right internal jugular vein before induction of general anesthesia.In group 2 and 4 an epidural catheter was inserted at T_(7-8) or T_(8-9) and advanced 3 .5-4.0 cm in the epidural spacecephalad. Epidural block was produced by a bolus of 0.5 % ropivacaine 7-9 ml followed by continuous infusion of0. 5 % ropivacaine at 3-5 ml?h~(-1). Anesthesia was induced with propofol 1 .0-1. 5 mg?kg~(-1), fentanyl 3?g?kg~(-1) andvecuronium 0. 1 mg?kg~(-1). A left-sided double-lumen tube was inserted and correct position was confirmed. Thepatients were mechenically ventilated. The ventilation collditions were FiO_2 = 100 %, V_T = 8-10 ml?kg~(-1), I: E =1: 5 and respiratory rate was adjusted to maintained P_(ET) CO_2 at 35-45 mm Hg during both two-lung ventilation(TLV) and OLV. Anesthesia was maintained with isoflurane inhalation in group 1 and 2 or continuous infusion ofpropofol in group 3 and 4 supplemented with intermittent i. v. boluses of fentanyl. MAP, HR, ECG, MPAP,CVP, continuous cardiac output (CCO), BIS and TOF were continuously monitored during anesthesia. BIS was maintained at 45-55. Arterial and pulmonary blood gases were analyzed before induction of anesthesia (T_1), 30min after TLV was started (T_2 ), and 5, 15, 30, 60, 120 and 180 min after OLV was started (T_(3-8)) and 30 minafter TLV was resumed (T_9 ). The Qs/Qt (shunt fraction) was calculated at T_(1-9) Results Qs/Qt was significantlyincreased after induction of general anesthesia and mechanical ventilation and increased further during OLVcompared with the baseline value (T_1) in all four groups. The calculated Qs/Qt values were highest at 15 min (T_4)or 30 min (T_5) of OLV and remained high for 30-60 min and then gradually decreasing. During OLV QS/Qt washigher in group 1 than in the other three groups (P0.05). Cardiac output was significantly higher in group 1 and 2 than thatin group 3 and 4 during OLV. Conclusion During prolonged OLV intrapulmonary shunt tends to decrease withincreasing oxygenation with time, regardless of anesthetic techniques employed. Isoflurane inhalation is associatedwith a signifficant increase in shunt fraction. Combined general and epidural anesthesia may induce greaterhemodynamic changes.

Objective To assess the mechanisms that contribute to lung injury in patients undergoing heart valve replacement with cardiopulmonary bypass (CPB) .Methods Eight HYHA grade Ⅱ-Ⅲ patients (4 males, 4 females) aged 47-67 years weighing 49.4-68.6 kg undergoing heart valve replacement with CPB were studied. The patients were premedicated with intramuscular morphine 0.1-0.2 mg?kg-1 and scopolamine 0.3 tng. Anesthesia was induced with midazolam 0.05-0.1 mg? kg-1 , fentanyl 15-20 ?g?kg-1 and pipecuronium 0.1 mg?kg-1 and maintained with intermittent Ⅳ boluses of midazolam 0.05 mg?kg-1 , fentanyl 10-30?g?kg-1 and pipecuronium 2 mg. Swan-Ganz catheter was placed via internal jugular vein after induction of anesthesia. Operation was performed under mild hypothermic (28-32℃) CPB. Blood samples were taken from radial and pulmonary artery for blood gas analysis and determination of neutrophil (PMN) counts, plasma TNFa and LPO concentrations and SOD activity prior to CPB (T0), 5 min after venae cava declamping (T1) and at the end of CPB (T2) and operation (T3 ) . The differences in the variables measured between pulmonary artery and vein were calculated to show the PMN entrapped, TNFa produced, SOD depleted and LPO released in the lungs. The alveolar-arterial oxygen tension difference (PA-aDO2) and intrapulmonary shunt( QS/QT)were calculated. Lung ischemia time was defined as the duration between occlusion and release of vena cava superior and inferior. Results The mean lung ischemia time was (97?21)min. MPAP, PVRI, PA-a.DO2 and QS/QT significantly increased after CPB, while PaO2/FiO2 and lung compliance significantly decreased compared with those before CPB (P

Objective To assess the influence of upper thoracic epidural anesthesia (TEA) on systemic oxygen supply-demand relationship during one-lung ventilation (OLV). Methods Twenty ASA Ⅰ-Ⅲ patients undergoing elective esophageal surgery were randomly divided into 2 groups : group Ⅰ general anesthesia (GI n = 10) and group Ⅱ combined general-epidural anesthesia (GIE n = 10). In both groups anesthesia was induced with propofol 1.5-2.0 mg?kg-1, fentanyl 3 ?g?kg-1 and vecuronium 0.1 mg?kg-1. The patients were intubated with double-lumen catheter. Correct positioning was verified by auscultation and fiberoptic bronchoscopy. Anesthesia was maintained with isoflurane (1.5-2.0% ) and intermittent i. v. boluses of fentanyl. BIS was maintained at 45-55 during operation. In GIE group epidural puncture was performed at T7-8 or T8-9. The catheter was advanced 3.5-4.0 ml in the epidural space cephalad. 0.5% ropivacaine was infused at 3-5 ml?h-1 during operation. Anesthetic block levels ranged from T2-4 to T10-12 . Radial artery was cannulated for BP monitoring and blood sampling and Swan-Ganz catheter was positioned in the pulmonary artery via right internal jugular vein. ECG, MAP, HR, CVP, continuous cardiac output index (CCI) and BIS were continuously monitored during anesthesia. Arterial and mixed venous blood samples were obtained before induction of anesthesia (T0 ), 30 min after intubation while two lungs were being ventilated (T1) at 15, 30, 60 and 120 min of OLV (T2-3) and 30 min after TLV was resumed (T6 ) . MAP, CVP, cardiac output index (CI) and arterial and mixed venous blood oxygen content were measured and oxygen supply (DO2) and consumption (VO2) were calculated at each time point. Results In GIE group MAP was significantly lower than that in GI group ( P 0.05). At 15, 30 and 60 min of OLV (T2-4) mixed venous oxygen saturation (SVO2 ) was significantly lower while VO2 significantly higher in group GIE than in group GI. Consequently DO2/ VO2 in group GIE was significantly lower than that in group GI. Conclusion Thoracic epidural anesthesia combined with general anesthesia increases oxygen consumption (VO2) and consequently decreases DO2/ VO2 during OLV.