BACKGROUND: Not only can auditory evoked potential (AEP) reflect electric activities of cerebral cortex and subcortex, but also have dose-effect relationship with many sorts of anesthesia agents; it is a relatively good index for monitoring anesthesia depth at present.OBJECTIVE: To analyze target controlled infusion propofol by auditory evoked potentials index during anaesthesia.DESIGN: Patients with operations were taken as objects in the randomized controlled trial.SETTING: Department of Anesthesia of Southwest Hospital of the Third Military Medical UniversityPARTICIPANTS: A total of 16 patients, with selective simply laparoscopic cholecystectomy, admitted to Department of Anesthesia of Southwest Hospital from October to November 2003, were selected and randomly divided into normal control group and auditory evoked potential index monitoring group with 8 in each group. The baseline information of the patients, such as gender, age, weight and operating time etc., was similar between the two groups (P ＞ 0.05).METHODS: Same anesthesia induction method was conducted on the patients in both groups; anesthesia was maintained with propofol (10 g/L) according to ALARIS P6003 pump calculation in the two groups; age, weight and target concentration of propofol (4 mg/L) was regulated according to clinical experience, while, in auditory evoked potential monitoring group,the concentration value of propofol in effective site was regulated by maintaining auditory evoked potential index between 15 and 30. Non-invasive blood pressure, heart rate and AAI were monitored at the moment of reposing for 10 minutes after entering operating room (T0), eyelash reflex disappearing after anaesthesia induction (T1), trachea intubation (T2), 3 minutes after intubation (T3), boring abdomenal holes (T4), 30 minutes after aeroperitonia steady (T5), observer's assessment of alertness and sedation (OAA/S) ≥4 at the end of operation (T6).MAIN OUTCOME MEASURES: ① Comparison of dosages of anaesthetia agents between the two groups. ② Changes of hemodynamics and auditory evoked potential index at each phase point. RESULTS: According to intention to treat analysis, all the 16 patients entered results analysis. ①Comparison of dosages of anesthesia agents between the patients in each two: The actual dosage of propofol in auditory evoked potential monitoring group was significantly lower than that in normal control group [(247.25±37.11), (337.38±36.72) mg, P ＜ 0.05], while the dosages of fentanyl and vecuronium bromide were no differences between two groups (P ＞ 0.05). ② Changes of hemodynamics and auditory eyoked potential index at each phase points of the two groups: Changes of hemodynamics at each phase points were similar between the two groups (P ＞ 0.05). Compared with T0 phase, there was no significant difference in auditory evoked potential index between the two groups in T1, T2 and T3 phases (P ＞ 0.05), however, in T4 and T5 phases, auditory evoked potential index in auditory evoked potential monitoring group was remarkably higher than that in normal control group (28.50±6.19, 21.25±4.06; 28.00±5.66,20.75±3.41; P ＜ 0.05). All patients had no awareness during the operation. CONCLUSION: Auditory evoked potential index is a new indicator for monitoring anesthesia depth, which can be helpful to regulate and control depth of anesthesia so as to avoid awareness and recall during general anesthesia.

Objective To evaluate the effect of ulinastatin on brain injury induced by lipopolysaccharide (LPS) in mice.Methods Ninety adult male C57 mice,aged 3-4 months,weighing 200-300 g,were randomly divided into 3 groups (n =30 each) using a random number table:control group (C group),LPS group and ulinastatin group (U group).Group U received intraperitoneal injection of ulinastatin 10 000 U/kg,while group L received the equal volume of normal saline,and 10 min later brain injury was produced with LPS 1 μg/g injected into the cerebral ventricle.Ten animals were chosen and blood samples were taken for determination of plasma concentrations of S100β protein and neuron-specific enolase (NSE) at 1,3 and 7 days after LPS injection.Then the animals were sacrificed and hippocampal tissues were obtained for determination of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α) contents and IL-1β mRNA and TNF-α mRNA expression.Results Compared with C group,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased at 1,3 and 7 days after LPS injection,and IL-1β mRNA and TNF-α mRNA expression was up-regulated at 1 and 3 days after LPS injection in LPS and U groups.Compared with group LPS,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased,and IL-1β mRNA and TNF-α mRNA expression was down-regulated at 1 and 3 days after LPS injection in group U.Conclusion Ulinastatin can attenuate brain injury induced by LPS in mice,and the mechanism is related to inhibited inflammatory responses.

0.05), the ratio of Cm/Cps rose gradually with lowering of rectal temperature and it reached the top value at 28℃; during this period AST, ALT, Cr and BUN decreased with dropping of rectal temperature (P

Objective To observe the changes of blood fentanyl concentration in rats during anhepatic phase by treatment of large dose of dexamethasone and to investigate the extrahepatic metabolism of fentanyl. Methods Thirty rats were randomly divided into 3 groups (n=10 in each group): normal control group (Group A), anhepatic phase group (Group B), anhepatic phase+dexamethasone treatment group (Group C). The hepatic portal of rats was dissociated and closed in Group B. In Group C, 20 mg/kg of dexamethasone was infused 1 h before the occlusion of hepatic portal. After intravenous injection of 20 ?g/kg fentanyl each time, the blood samples were collected. The fentanyl blood concentration was analyzed by HPLC. Results The blood fentanyl concentration of anhepatic phase dropped more slowly in Group B than Group C (P0.05). Conclusion The liver is the main organ for fentanyl metabolism. There is the extrahepatic metabolism for fentanyl and dexamethasone can enhance the extrahepatic metabolism of fentanyl.

Objective To investigate the role of intercellular adhesion molecule-1(ICAM-1)in Isoflurane against hepatic ischemia-reperfusion(I/R)injury in vivo.Methods Thirty-two female SD rats were randomly divided into 4 groups:sham-operation group(A),I/R group(B),Isoflurane group(C),I/R+ Isoflurane group(D).Groups A and C were be used as controls.In groups B and C,the hepatic hilar vessels distributing to the left and median lobes were clamped to induce partial hepatic ischemia(70%).Reperfusion was done 60 min after hepatic ischemia.The animals were killed 3 h after reperfusion,then the specimens of liver tissues and blood were obtained.ALT and AST in blood serum were detected as liver damage markers.The histological examination of liver tissues was done by hematoxylin and eosin staining.The levels of ICAM-1 protein in the hepatic tissues were detected by immunohistochemistry.Results After hepatic ischemia-reperfusion,the ICAM-1 protein expression in the hepatic tissues increased;ALT and AST increased;Reperfusion induced severe liver damage.Isoflurane significantly inhibited the ICAM-1 expression.Conclusion The degree of hepatic ischemia-reperfusion injury is closely associated with the expression level of ICAM-1.Isoflurane abates liver ischemia-reperfusion injury and inhibits the ICAM-1 expression.

Objective To investigate the effect of nalmefene on the cerebral ischemia-reperfusion (I/R) injury in rats.Methods Forty-eight male Sprague-Dawley rats, aged 3-4 months, weighing 220260 g, were randomly allocated to control group (group C), sham operation group (group S), cerebral I/R group (group I/R), or nalmefene group (group N) using a random number table, with 12 rats in each group.Cerebral I/R was induced by occlusion of bilateral common carotid arteries for 20 min followed by reperfusion.Group C received no treatment.Group S underwent 20 min exposure of bilateral common carotid arteries and then received suture.In group N, nalmefene 0.1 mg/kg was injected intraperitoneally immediately after reperfusion.At 6, 24 and 72 h of reperfusion, venous blood samples were collected for determination of the concentrations of S-100β protein and neuron-specific enolase (NSE) in plasma by enzyme-linked immunosorbent assay.After the last blood sampling, the rats were sacrificed, and brains were removed for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) contents in brain tissues by enzyme-linked immunosorbent assay.Results Compared with group C, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1βcontents in brain tissues were significantly increased in S and I/R groups (P＜0.01).Compared with group S, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1β contents in brain tissues were significantly increased in group I/R (P＜0.01).Compared with group I/R, the plasma S-100β protein and NSE concentrations at each time point of reperfusion, and TNF-α and IL-1β contents in brain tissues were significantly decreased in group N (P ＜ 0.01).Conclusion Nalmefene can mitigate cerebral I/R injury in rats.

Objective Aprotinin, a serine proteinase inhibitor, has been reported to reduce blood loss significantly in patients undergoing cardiac surgery with CPB, heart and liver transplantation. The aim of this study was to evaluate the effect of aprotinin on intraoperative blood loss, transfusion requirement and blood coagulation during liver cancer resection.Methods Eighty-two ASA Ⅰ -Ⅲ patients ( 51 male, 31 female ) aged 33-65 yr undergoing liver cancer resection ( 61 partial hepatectomy, 21 extirpation of liver cancer) were studied. The patients were randomly divided into 2 groups : aprotinin group received a bolus of aprotinin 1 112 EPU after induction of anesthesia, followed by continuous aprotinin infusion at 278 EPU?h-1 until 2 h after operation ( n = 40); control group received normal saline instead of aprotinin ( n = 42) . The patients were premedicated with sodium luminal, droperidol-fentanyl and atropine. Anesthesia was induced with midazolam 2 mg, thiopental 5 mg?kg-1 and succinylcholine 1.5 mg? kg-1 . After tracheal intubation the patient was mechanically ventilated (VT = 8-12 ml?kg-1 ) and PaCO2 was maintained at about 35 mm Hg, Anesthesia was maintained with N2O/O2 , fentanyl and vecuroniurn. Venous blood samples were taken before induction of anesthesia (baseline) , 0.5 h, 2 h and 4 h after skin incision and 6 h and 12 h after operation for routine blood tests, thromboelastography ( TEG), and determination of activated partial thromboplastin time (APTT), thromboplastin time (TT) prothrombin time (PT) and plasma fibrinogen concentration (Fig) . Intraoperative blood loss and amount of blood transfused were recorded. Results The preoperative hypercoagulable state was ameliorated and coagulation was maintained within the normal range in aprotinin group; while in control group the hypercoagulable state was aggravated during operation and at the end of operation it changed to hypocoagulable state. The intraoperative blood loss and amount of blood infused were significantly less in aprotinin group than in control group. Conclusion The use of aprotinin during liver cancer resection results in reduction in intraoperative blood loss and less transfusion requirement.

0.05). ② The depth of anesthesia: the value of AEP index in AEP index group was significantly higher than that in control group ( P

Objective To study the possible mechanisms of aprotinin in the protection of platelets. Methods Cytosolic free calcium concentration ([Ca 2+ ]i) was determined in calcium fluorescent indicator Fura 2/AM loaded washed human platelets by using dual wavelength spectrofluorophotometer. The mean value of resting [Ca 2+ ]i and the changes of [Ca 2+ ]i response to thrombin and aprotinin were observed. Results In the presence of extracellular Ca 2+ at the dose of 1 mmol/L, the resting level of [Ca 2+ ]i in platelets of human was (151.840?28.719) nmol/L. Thrombin stimulated the rise in [Ca 2+ ]i in the presence of Ca 2+ at the dose of 1 mmol/L, and the effects were inhibited by aprotinin in a concentration dependent manner ( P

The effects of ketamine on the hemodynamics in the postshock stage in 10 severely burn patients were observed.Their average burn area was 53.7?14% TBSA.Anesthesia was inducedwith 2 mg/kg of ketamine and then maintained with 50?g/kg/minute of ketamine.All the patients kept on spontaneous breathing.Measurements were performed before anesthesia,5 and 30 minutes after the induction of anesthesia.and 20 minutes after the discontinuation of ketamine.Our findings indicate that the severely burn patients in the postshock stage were in a state of active hemodynamics with increased cardiac output and decreased peripheral resistance.The plasma concentrations of epinephrine and norepinephrine were apparently increased.A small dose of ketamine could further increase the release of epinephrine,which is beneficial to the restoration of normal cardiovascular functions.