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 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.

Objective To evaluate the ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion (I/R) in rats.Methods Ninety adult male Sprague-Dawley rats,aged 350-450 g,were randomly divided into 3 groups (n =30 each) using a random number table:sham operation group (S group),I/R group,and ischemic postconditioning group (group P).Focal cerebral I/R was induced by electrocoagulation of left middle cerebral artery and 30 min occlusion of bilateral common carotid arteries followed by reperfusion.In group P,bilateral common carotid arteries were subjected to 3 cycles of 30 s reperfusion and 10 s ischemia at the beginning of reperfusion.At 24 h of reperfusion,neurological deficit was scored,and cerebral infarct size was detected by TTC staining.At 6,12 and 24 h of reperfusion,the expression of glucose-regulated protein 78 (GRP78),C/EBP homologous protein (CHOP) and caspase-12 in the ischemic area were measured (using immunohistochemistry).The neuronal apoptosis in the ischemic area was detected by TUNEL.Results Compared with S group,the neurological deficit score was significantly increased,cerebral infarct size was enlarged,the neuronal apoptosis was increased,and the expression of GRP78,CHOP and caspase-12 was up-regulated in I/R and P groups.The neurological deficit score was significantly lower,cerebral infarct size was smaller,the expression of GRP78 was higher at 12 and 24 h of reperfusion,the neuronal apoptosis was lower at 24 h of reperfusion,and the expression of CHOP and caspase-12 was lower in group P than in group I/R.Concluion Ischemic postconditioning can inhibit neuronal apoptosis mediated by endoplasmic reticulum stress during cerebral I/R,which dose not play a leading role in cerebral protection in rats.

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 explore the relationship between Bispectral index （BIS） values,Narcotrend index （NTI） values and the predicted effect-site concentration （EC）during target-controlled infusion of propofol. Methods In 30 patients during target-controlled infusion of propofol,the propofol infusion was set at an initial EC of 0.5 mg/L and increased by 0.5 mg/L steps every 5 min until 5 min after the modified observer＇s assessment of alertness/sedation scale（OAA/S） values reached zero. The predicted EC of propofol,the values of NTI,NTS and BIS were recorded,and the sedation level were examined by the modified OAA/S every 20 s. The predicted EC of propofol and the values of BIS and NTI at LVC and LOC in 5%,50% and 95% of patients were calculated. Results There were good linear correlations between BIS,NTI and the predicted EC of propofol （r2=0.787,0.792）.The predicted EC of propofol at LVC in 5%,50% and 95% of patients were 1.2,1.8 and 2.5 mg/L,respectively. The values of BIS and NTI at LVC in 5%,50% and 95% of patients were 78.2,68.2 and 58.2; 73.9,64.9 and 55.8,respectively.The predicted EC of propofol at LOC in 5%,50% and 95% of patients were 1.6,2.6 and 3.5 mg/L,The values of BIS and NTI at LOC in 5%,50% and 95% of patients were 74.6,58.2 and 41.5,66.2,55.8 and 45.3,respectively. Conclusion During target-controlled infusion of propofol,LVC and LOC occurred within a definite range of predicted effect-site concentrations.There were the good linear correlations between BIS,NTI and the predicted EC of propofol.NTI may be more useful than BIS in predicting LVC and LOC because of the smaller range of values for the two clinical end-points.

Objective To observe the effects of sulfentanil with various doses on the Bispectral index and Narcotrend index without nociceptive stimulus under the sevoflurane anesthesia.Methods Forty-eight ASA Ⅰ or Ⅱ patients undergoing gynecological operations were randomly divided into four groups（n=12）.All patients were induced with sevoflurane,the end-tidal concentrations of sevoflurane in all groups were adjusted to 1.0 MAC after tracheal intubation. Fifteen minutes later,sufentanil was injected in groups of B,C,D with the doses of 0.25,0.5,1.0 μg/kg respectively. The observations were finished when the values of Bispectral index and the Narcotrend index reached the minimum over 5 min. The values of Bispectral index and the Narcotrend index were recorded every minutes after the sufentanil injection. Results Among all groups,the BIS,Narcotrend values and tmax produced no statistical difference. Compared with the time when conscious lost,BIS and Narcotrend values were significantly lower when sevoflurane anesthesia reached steady state in all groups. The values of BIS and Narcotrend were significant lower after the injection of sufentanil in the groups of B,C and D（P0.05）. Conclusion Under the sevoflurane anesthesia with the steady end-tidal concentration of 1.0MAC,sufentanil could reduce the values of BIS and Narcotrend index without nociceptive stimulus without distinction among different doses.

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

Objective To investigate the effects of continuous spinal anesthesia with different concentrations and doses of ropivacaine on the ultrastructure of the spinal cord and nerve roots. Methods Twenty-four male SD rats weighing 220-280 g were anesthetized with intraperitoneal 10% chloral hydrate 300-350 mg/kg. A polyurethane microcatheter was inserted into the lumbar subarachnoid space according to the technique described by Yaksh. An 8-cm catheter segment was left in the subarachnoid space. The animals were randomized to receive normal saline, 0.5%, 0.75% or 1.0% ropivacaine 40 ? 1 intrathecally 3 times at 1.5 h interval. Six hours after the first intrathecal administration the animals were decapitated and L1 ,2 segment of the spinal cord and nerve roots were immediately removed for electron microscopic examination. Results Electron microscopic examination revealed that in animals which received intrathecal (i.t.) normal saline, 0.5% or 0.75% ropivacaine the neurolemma of the nerve roots and the mitochondria and endoplasmic reticulum of the neurons in the spinal cord were intact, while in animals which received i.t. 1.0% ropivacaine the neurolemma was stratified and partly disrupted and there were swelling of endoplasmic reticulum and vacuole degeneration. Conclusion Six hours continuous spinal anesthesia with 1.0% ropivacaine may be injurious to the spinal cord and nerve roots.

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.