Objective To investigate the change in neuromuscular blocking effect of rocuronium induced by liver dysfunction. Methods Forty patients undergoing elective liver and biliary tract operation under general anesthesia were divided into 2 groups : (A) control group included 20 patients with normal liver function and (B) liver dysfunction group included 20 patients with obstructive jaundice. The premedication consisted of phenobarbital 0.lg and atropine 0.5 mg. Anesthesia was induced with midazolam 0.1 mg?kg-1,fentanyl 6?g?kg-1 and etomidate 0.3 mg?kg-1.The neuromuscular function was monitored by TOF stimulation of the ulnar nerve using accelerograph (Biometer).Rocuronium 0.6 mg?kg-1 was administered iv via the vein in the upper arm.The patients were intubated when T1 was 95% depressed and mechanically ventilated.PETCO2 was maintained at 35-40 mm Hg.The onset time (from the end of injection to T1=0),clinical duration of action (from the end of injection to 25% recovery of T1) and recovery index (T1 from 25% to 95% ) were recorded.MAP, HR and SpO2 were recorded before and at 5 and 10 min after rocuronium injection.Results The demographic data including sex, age and weight were comparable between the two groups. The onset time was (63?19) s in group A and (70?21) s in group B.The difference was not statistically significant. The clinical duration of action was (41?16) min in group A and (67?29) min in group B (P0.05).Conclusion Liver dysfunction induced by obstructive jaundice prolongs the clinical duration of action,but does not significantly affect the onset time of and recovery from rocuronium.

ve To investigate the time course of potentiation of rocuronium produced by 1MAC of desflurane or isoflurane. Methods Twenty-four ASA I-II patients aged 18-60 years undergoing elective abdominal operation under general anesthesia were studied. Patients with neuromuscular, liver or kidney disease and those receiving any drug which may affect neuromuscular transmission were excluded. Premedication consisted of intramuscular phenobarbital 0.1 and atropine 0.5mg 30min before operation. Anesthesia was induced with midazolam 0.1-0.2 mg?kg-1, fentanyl 6?g.kg-1 and etomidate 0.3mg?kg-1 .Tracheal intubation was facilitated with rocuronium 0.6mg?kg-1 iv. The degree of neuromuscular block was monitored by measuring muscle response to TOF using accelerography (Biometer) . For maintenance of anesthesia the patients were randomly assigned to receive either propofol + fentanyl (control group) or 1 MAC of desflurane + propofol + fentanyl (desflurane group) or 1 MAC of isoflurane + propofol + fentanyl(isoflurane group). Rocuronium was continuously infused during operation to maintain T1 at 5 % of the control and the infusion rate was recorded every 15 min. Results There were no significant differences among the three groups with respect to sex, age, body weight and duration of anesthesia. In Des and Iso groups the infusion rate of rocuronium was reduced in an exponential manner and maximal potentiation occurred at 90 min of isoflurane or desflurane inhalation. The maximal reduction in infusion rate was 42.7 % in Des group and 37.6% in Iso group. There was no significant difference between the two groups.Conclusions Desflurane and isoflurane can potentiate the muscle relaxation produced by rocuronium in a similar degree and the potentiation is time dependent.

Objective To compare the efficacy of sevoflurane inhalation and remifentanil-propofol anesthesia in patients undergoing total gastrectomy. Methods Forty ASA class Ⅰ or Ⅱ patients with gastric cancer were divided into sevoflurane inhalation anesthesia (group S) and remifentanil-propofol intravenous anesthesia(group P), with 20 cases each. Perioperative hemodynamic veriables, bispectral index (BIS) values and end-tidal concentration of sevoflurane were continuously monitored. The time of recovery from anesthesia and adverse reactions of anesthesia were recorded as well. Results Compared with those before anesthesia, BP and HR were significantly decreased (P< 0. 05). The depth of anesthesia in both groups was maintained well with BIS in 45-60 and vital signs were stable during operation. The recovery from anesthesia was quicker in group P than that in group S. The incidences of restlessness and couphing were obviously lower in group P than those in group S (P<0.05). Conclusion Either sevoflurane inhalation or remifentanil-propofol intravenous anesthesia can be used safely in total gastrectomy.

Objective To evaluate the accuracy of BIS and anesthetic depth index (CSI) for monitoring levels of sedation induced by different target effect-site concentrations (CT) during TCI of propofol combined with sufentanil. Methods Ninety ASA Ⅰ or Ⅱ patients of both sexes aged 20-49 yr weighing 45-70 kg undergoing elective surgery under general anesthesia were randomly divided into 6 groups (n=15 each): group Ⅰ, Ⅱ, Ⅲ TCI of propofol with CT set at 2, 4 and 6 μg/ml respectively (P1-3);groupⅣ, Ⅴ,Ⅵ sufentanil 0.7 μg/kg + propefol TCI with CT set at 2, 4 and 6 μg/ml (SP1-3). Anesthesia was induced with propefol TCI with CT set at 4 μg/ml in all 6 groups. As soon as the patients lost consciousness, tracheal intubation was facilitated with vecuronium 0.1 mg/kg. The patients were mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with propofol TCI with CT set at 2 μg/ml(in group P1, SP1), 4 μg/ml(in group P2, SP2) and 6 μg/ml(in group P3,SP3) immediately after intubation respectively. Sufentanil 0.7 μg/kg was given iv at 20 min after propofol TCI was started in group SP<1-3. MAP, HR, BIS (Aspect) and CSI (Danmeter Denmark) were continuously monitored and recorded before induction of anesthesia (T0, baseline), at 1 min before tracheal intubation (T1), and at 30 s(T2), 15 min(T3), 30 min(T4), 35 min(T5) and 40 min (T6) after tracheal intubation. Results BIS and CSI values were gradually decreasing at T3-6 in group P1-3 and SP1-3. BIS and CSI values were significantly lower at T4-6 in group SP1 and SP2 than in group P1 and P2. CSI values were significantly lower at T4-6 in group SP3 than in group P3, but there was no significant difference in BIS values at T4-6 between SP3 and P3. Conclusion CSI and BIS can monitor the levels of sedation indueed with TCI of propofol with CT set at 2 and 4 μg/ml when combined with sufentanil 0.7 μg/kg but only CSI can monitor the level of sedation induced by propofol TCI with CT set at 6 μg/ml when combined with sufentanil 0.7 μg/kg.

Objective To investigate the effects of sevoflurane preconditioning (SP) on acute lung injury induced by lipopolysaccharide (LPS) in rats.Methods Twenty-four male SD rats weighing 220-250 g were randomly divided into 4 groups (n = 6 each): group Ⅰ control (group C),group Ⅱ LPS,group Ⅲ sevoflurane (group Sev) and group Ⅳ SP + LPS.In group Ⅰ and Ⅱ ,normal saline and LPS 5 mg/kg were given Ⅳ 30 min after ventilation respectively.In group Ⅲ and Ⅳ,the animals inhaled sevoflurane (end-tidal concentration 2.4% ) for 30 min followed by 5 min wash-out,and then received iv injection of normal saline and LPS 5 mg/kg respectively.The animals were killed at 6 h after LPS or normal saline administration.Lungs were removed for determination of W/D lung weight ratio,myeloperoxidase (MPO) activity,cytokine-induced neutrophil chemoattractant-1 (CINC-1) content and expression of CINC-1 and CINC-1 mRNA.The severity of lung injury was evaluated using diffuse alveolar damage (DAD) score.Results Compared with group Ⅰ ,W/D lung weight ratio,DAD score,MPO activity and CINC-1 content were significantly increased,and expression of CINC-1 and CINC-1 mRNA up-regulated in group Ⅱ and Ⅲ,while there was no significant difference in the above indices between group Ⅲ and group Ⅰ .Compared with group Ⅱ ,W/D lung weight ratio,DAD score,MPO activity and CINC-1 content were significantly decreased,and expression of CINC-1 and CINC-1 mRNA down-regulated in group Ⅲ.Conclusion Sevoflurane preconditioning can protect the lungs against LPS-induced acute lung injury by inhibiting inflaunnatory response.

Objective To compare the accuracy of bispectral index (BIS) and cerebral state index (CSI) used to measure depth of sedation during target-controlled infusion (TCI) of propofol. Methods After obtaining written informed consent we studied 20 ASA Ⅰ-Ⅱ patients aged 25-40 years undergoing elective operation under general anesthesia. The patients were premedicated with intramuscular atropine 0.5 mg. The electrodes of BIS and CSI were placed according to the instruction manuals before induction of anesthesia. Anesthesia was induced with TCI of propofol. The target effect-site concentration was set initially at 0.5 ?g?ml-1 followed by increments of 0.5 ?g?ml-1 every 5 min until 5 min after the patients lost consciousness and did not respond to pain stimulation (OAA/S= 0) . BIS and CSI were continuously monitored and their values recorded every 2-6 seconds. OAA/S score (5 = alert, 1 = loss of consciousness) was recorded every 20 seconds. Spearman correlation coefficient between OAA/S score and BIS and CSI and their prediction probabilities (Pk) were calculated. BIS05, BIS50, BIS95 and CSI05, CSI50, CSI95 at loss of consciousness (LOC) (OAA/S = 1) were also calculated.Results CSI arid BIS correlated well with sedation depth. There was no significant difference in the prediction probability between CSI and BIS. BIS05 and CSI05 were 79.1 and 74.9; BIS50 and CSI50 67.5 and 65.9; BIS95 and CSI95 55.9 and 56.8 respectively at LOC. Conclusion During TCI of propofol both CSI and BIS can be used to measure sedation depth fairly accurately. CSI appears to be more accurate then BIS in predicting both loss of verbal contact and LOC.

Objective To study the effects of glycyrrhizin on cerebral mitochondrial ATPase and membrane fluidity and malondialdehyde (MDA) and water content and brain function after cardiac arrest and resuscitation.Methods Eighteen dogs weighing 10-14 kg were randomly divided into 3 groups ( n = 6 each) : group A control; group B cardiac arrest and resuscitation and group C glycyrrhizin + cardiac arrest and resuscitation. The animals were anesthetized with fentanyl, intubated and mechanically ventilated and PaCO2 was maintained within normal range. The chest was opened. In group B and C cardiac arrest was produced by clamping of ascending aorta and coronary perfusion with hyperkalemic cardioplegic solution and maintained for 18 min and resuscitated by direct cardiac massage, adrenaline and defibrillation. The animals were observed for 8 h after spontaneous cardiac rhythm resumed. In group C glycyrrhizin injectio 40 ml?kg-1 was infused over 8 h as soon as spontaneous cardiac rhythm resumed. Brain function was evaluated according to Pittsburgh Brain stem score (PBSS). The animals were then killed and their brains removed for determination of (1) mitochondrial membrane fluidity and Na+-K+-ATPase and Mg2+ -ATPase activity and (2) brain MDA and water content.Results The mitochondrial membrane viscosity and cerebral MDA and water content were significantly higher and ATPase activity was significantly lower in group B (cardiac arrest) than in group A (control) . Brain function was also impaired by global cerebral ischemia-reperfusion (I/R) in group B. In group C glycyrrhizin infusion significantly attenuated the deleterious effects of cerebral I/R by reducing mitochondrial membrane viscosity and cerebral MDA and water content and increasing ATPase activity. Glycyrrhizin infusion also improved brain function.Conclusion Glycyrrhizin can ameliorate the deleterious effects of global cerebral I/R induced by cardiac arrest.

Objective To study the effects of selective mild cerebral hypothermia on endogenous anti-injury mechanism in brain tissue after cardiac arrest and resuscitation. Methods Fifteen healthy mongrel dogs of both sexes were anesthetized and intubated. Cardiac arrest was induced by potassium cardioplegia and cross-clamping of aorta, vena cava superior and inferior and azygos vein and maintained for 18min. The animals were randomly divided into 3 groups: group A, in which no cardiac arrest was induced, served as control ( n = 4) ; in group B animals received routine cerebral resuscitation ( n = 5) ; in group C animals received selective mild cerebral hypothermia (34℃?0.5℃) and routine cerebral resuscitation ( n = 6) . After successful resuscitation, the animals were observed for 8 hours. At the end of the experiment the parietal cerebral cortex was removed for determination of MDA, GSH, LA, FFA content and activities of SOD(T-SOD, Mn-SOD, Cu-ZnSOD) and GSH-Px. Results FFA and LA content of brain tissue in group B was significantly higher than those in group A (P

Objective To observe the effects of polyglucose and sodium chloride injection on treating hypotension of patients in postanesthesia care unit (PACU).Methods Everyone of thirty-two patients with hypotension in PACU received 500ml polyglucose and sodium chloride injection by venous injection at the velocity of 12ml?kg -1 ?h -1 .The mean arterial pressure (MAP),heart rate (HR) were recorded before administration and 5, 15,30,60 min after administration, the urine volume was measured at 1 hour after administration ,and the blood gas analysis were measured before injection and an hour after injection.Results The MAP increased significantly at 5min after administration,and the effects could last 60 minutes, the urine volume increased and the Hb and K + reduced remarkable after injection.Conclusions The administration of polyglucose and sodium chloride injection can effectively increase blood volume and blood pressure,and reduce blood transfusion,so might reduce complications of blood transfusion. [

Objective To investigate the effects of intrathecal morphine on cell-mediated immunity. Methods Forty male SD rats weighing 250-300 g were randomly divided into 5 groups ( n = 8 in each group) : sham-operated group (F); saline group (NS) and 3 morphine groups (M1, M2, M3). The animals were anesthetized with intraperitoneal chloral hydrate 300-350 mg?kg-1 . Microspinal catheter was inserted into the subarachnoid space at the lumbar region according to modified Yaksh technique. Correct implantation of the spinal catheter was confirmed by aspiration of CSF. In the morphine groups, after 5 days morphine was continuously infused through the spinal catheter at 2.5 (Ml), 5.0 (M2) and 10 ?g?h-1(M3) for 7 days. In NS group normal saline was continuously infused instead of morphine. On the 7th day 5% formalin 50 fd was injected into the plantar surface of left hindpaw. The number of flinches, lickings and total time of licking were recorded for 60 min. Pain intensity scoring (PIS) (0-3, 0 = no pain, 3 = severe pain) was used to assess the antinociceptive effect of intrathecal morphine. The animals were killed after evaluation of pain intensity. Body weight and spleen weight were measured. Spleen index (spleen weight/body weight) was calculated. T-lymphocyte function was evaluated based on Concanavalin-A (Con A) induced splenocyte proliferation. Modified lactic acid dehydrogenase (LDH) release assay was used to assess NK cell activity. Results The PIS scores were significantly lower in group M1 , M2 and M3 than in F and NS group. The spleen index, splenocyte proliferation induced by Con A and NK cell activity were significantly suppressed in the 3 morphine groups Conclusion Intrathecal morphine has significant antinociceptive effect and suppresses T-lymphocyte proliferation and NK cell activity in a dose-dependent manner