Objective To evaluate the role of autophagy in apoptosis in cortical neurons of rats in the early phase of oxygen-glucose deprivation (OGD).Methods Female Sprague-Dawley rats at 16-18 days of gestation,weighing 350-400 g,were sacrificed after being anesthetized with pentobarbital sodium.The fetal rats were obtained and the primary cortical neurons were isolated and seeded in culture plates.The neurons were then divided into 4 groups (n =7 each) using a random number table:control group (group C),OGD 30 min group,OGD 1 h group,OGD 2 h group,and OGD 3 h group,OGD + autophagy inducer rapamycin group (OGD + R group),and OGD + autophagy inhibitor 3-methyladenine (3-MA) group (OGD + 3-MA group).The neurons were incubated in sugar-free DMEM medium containing 5％ CO2 and 95％ N2 for 30 min,1,2 and 3 h in OGD 30 min,1 h,2 h,and 3 h groups,respectively.Rapamycin (final concentration of 100 nmol/L) and 3-MA (final concentration of 10 mmol/L) were added to sugar-free DMEM medium in OGD + R and OGD + 3-MA groups,respectively,and the neurons were then incubated for 1 h.The CCK-8 assay was used to detect the neuronal viability after the end of OGD.The expression of caspase-3 and LC3 Ⅱ was measured by Western blot.Results Compared with C group,the survival rates of cortical neurons were significantly decreased in the other groups,the expression of LC3 Ⅱ was up-regulated in OGD 30 min,1 h,2 h and 3 h groups,no significant change was found in caspase-3 expression in OGD + R group,and the expression of caspase-3 was up-regulated in the other groups.Compared with OGD 1 h group,the survival rates of cortical neurons were significantly decreased in OGD2 h,OGD3 h and OGD + 3-MA groups,the survival rates of cortical neurons were increased,and the expression of caspase-3 was down-regulated in OGD + R group,the expression of LC3 Ⅱ was up-regulated in OGD + 3-MA group,and the expression of LC3 Ⅱ was down-regulated in OGD2 h and 3 h groups.Conclusion Autophagy initiated in the early phase of OGD can inhibit apoptosis in cortical neurons of fetal rats.

Immune response after blood transfusion is closely related to prognosis of the patients receiving blood productions. Thus, the safety and effectiveness are paid increasing attention.This article reviews immunological consequence and clinical manifesta-tions and response strategies after transfusion, which aims to provide reference for clinical transfusion decisions.

Esophageal cancer is the leading cause of cancer-related deaths worldwide.A single intraoperative intervention is unlikely to benefit the outcome.A multimodal management plan that includes the use of TEA seems to demonstrate improved results in high-volume centers.Anesthetic management may contribute to the containment of pulmonary morbidity and anastomotic leakage by the use of TEA,protective ventilation strategies during OLV,prevention of tracheal aspiration,and judicious fluid management.

Objective To investigate the effects of ketamine on endotoxin-induced production of proinflammatory cytokines (IL-6, TNF-?) and activation of their modulating factor NF-?B in rat. Methods Thirty-six adult male Wistar rats weighing 250-300 g were randomly divided into 4 groups : (Ⅰ Ⅰ ) control group ( n = 6) ; (Ⅱ) endotoxin group received intravenous endotoxin ( Escherichia coli O111: B4)5mg?kg-1(n = 6); (Ⅲ) ketamine group received ketamine 50 mg?kg-1 ? h-1 i.v. (n = 6) and (Ⅳ) endotoxin + ketamine group received ketamine 0.5 or 5 or 50 mg?kg-1 ? h-1 after endotoxin ( n = 18 ) . The animals were anesthetized with urethane i. p. (1 g?kg-1) . Carotid artery was cannulated for BP and HR monitoring and jugular vein was cannulated for fluid or drug administration. Two hours after endotoxin administration the animals were sacrificed by exsanguination. Blood was collected and peripheral blood monocytes (PBMC) were isolated. NF-icB content in PBMC was measured by EMSA and plasma TNF-? and IL-6 concentrations were determined by ELISA. Results Progressive hypotension and tachycardia developed after endotoxin administration. Endotoxin also increased NF-icB content in PBMCs and plasma TNF-? and IL-6 concentrations. Ketamine 50 mg?kg-1 attenuated the endotoxin-induced hemodynamic response. Ketamine (0.5, 5, 50 mg?kg-1?h-1 ) suppressed NF-?B content in PBMC and inhibited plasma TNF-? level but plasma IL-6 level was not affected. Conclusion Ketamine can suppress endotoxin-induced NF-kappa B activation. Subanesthetic dose of ketamine has anti-inflammatory action.

Objective:To compare the cardiovascular effects of sufentanyl and fentanyl as combined with propofol in anesthesia during laparoscopic cholecystectomy(LC).Methods:Patients undergoing LC were randomly divided into two groups: 60 patients in the Sufentanyl group(group S,0.3 ?g/kg) and 53 patients in the Fentanyl group(group F,3 ?g/kg).The mean arterial pressure(MAP),heart rate(HR),cardiac output(CO),and cardiac index(CI) were recorded before induction,before pneumoperitoneum,after pneumoperitoneum and at the end of operation.Results:There was no difference in MAP,HR,CO or CI between the two groups before induction.The values of HR and CO increased significantly in group F after preumoperitoneum comparing with the values before preumoperitoneum(P

The effects of SHCDCT (selective head coolingdehydration combined therapy) on hypermetabolism, and its relation with thyroigenous hormones.The changes of glucose,phosphlipids,FT3 and TSH at 30, 180, 360 min of reperfusion following 30 min complete cerebral ischemia (four-vessel model ) in rabbits were observed.The effect of SHC (selective head cooling), DH(dehydration),SHCDCT on these changes were compared.SHC (28'C ) was induced by surface cooling methods.Compared with non-ischemia group,glouse, phospholipids decreased during reperfusoin,FT3 and TSH increased (P

Objective: To assess whether selective head cooling (SHC)could ameliorate the post-ischemie reperfusion injury. Method: Complete cerebral ischemia (CCI)was induced with the four vessel model for 30 min. 196 New Zealand rebbits were randomly allocated into three groups:group Ⅰ served as nonischemie control; animals in three subgroups of other groups had reperfused lasting 30,180 and 360 min respectively following CCI. Group Ⅱ served as normothermic reperfusion; group Ⅲ treated with selective head cooling(28℃,). Twenty-one endogenous parameters in brain were determined, and histomorphological assessment of neuronal chanes was observed. Neurons were classified respectively into type A(normal)and B(mild damage)etc. Result: As compared with group Ⅰ, the percentage of type A neurons was progressively decreased, while that of type B neurons increased sigmficantly in group Ⅰ (P

ObjectiveTo evaluate the effect of hydrogen-rich saline given during reperfusion on global cerebral ischeraia-reperfusion (I/R) injury in rats.Methods Seventy-two adult male SD rats,aged 2.0-2.5 months,weighing 260-300 g,were randomly divided into 3 groups (n ＝ 24 each):sham operation group (group S),group I/R and hydrogen-rich saline group (group H).In groups I/R and H cerebral I/R was induced by occlusion of 4 vessels( cauterization of bilateral carotid arteries and 15 min occlusion of bilateral common carotid arteries).In group H intraperitoneal 0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected at 6 h of reperfusion,while equal volume of normal saline was injected instead of hydrogen-rich saline.Eighteen rats of each group were sacririced at 24 h of reperfusion,and then the hippocampi were removed for determination of malondialdehyde (MDA),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6)contents,and nuclear factor-κB (NF-κB) activity and activated caspase-3 expression.Another six rats of each group were sacrificed at 72 h of reperfusion,and then brain tissues were removed for microscopic examination and counting the number of uninjured pyramidal cells in hippocampal CA1 region.ResultsCompared with S group,the contents of MDA,TNF-α,IL-6 and NF-κB activity were significantly increased,activated caspase-3 expression was significantly up-regulated,uninjured pyramidal cells in hippocampal CA1 region were significantly decreased in I/R group( P < 0.05).Hydrogen-rich saline given during reperfusion attenuated the above-mentioned I/R-induced changes( P < 0.05 ).The histologic damage of the hippocampal CA1 region was significantly slighter in group H than group I/R.ConclusionHydrogen-rich saline given during reperfusion can reduce global cerebral I/R injury in rats through inhibition of lipid peroxidation,inflammatory response and apoptosis.

Objective To explore the possible mechanism for the neuroprotective effect of ifenprodil by investigating its effects on inducible nitric oxide synthase (iNOS) expression and activity and apoptosis in the ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male SD rats weighing 280-320 g were randomly divided into 3 groups ( n = 18 each) : I sham operation group (group S) ; II focal cerebral I/R group (group I/R) and Ⅲ ifenpradil preconditioning group (group IF) received intraperitoneal ifenprodil 10 mg/kg before focal cerebral I/R. Focal cerebral I/R was induced by middle cerebral artery occlusion (MCAO) . A 3-0 nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. MCAO was maintained for 2 h. At 48 h after reperfusion, the animals were assessed for neurological function which was scored (0 = no functional deficit, 4 = unable to crawl, unconscious) and then decapitated. The brains were immediately removed for microscopic examination and determination of iNOS protein expression and activity, NO content and apoptosis in the ischemic core (IC) and penumbra (IP). Results Ifenprodil pretreatment significantly decreased the cerebral infarct size and neurological scores in group IF as compared with group I/R. In group I/R the iNOS activity was increased compared with group S.The iNOS activity and NO content were significantly lower in IP than in IC in group IR and IF. The TUNEL-positive cells were also mainly confined to IP. Compared with group I/R, in group IF the iNOS protein expression was significantly down-regulated in IC and IP and the iNOS activity and NO content in IC and IP were suppressed and TUNEL-positive cells were significantly reduced in IP. Conclusion Ifenprodil pretreatment has protective effect against cerebral I/R injury by inhibiting iNOS protein expression in IP, suppressing iNOS activity and NO content and reducing apoptosis.

Objective To investigate the effect of dezocine combined with sufentanil on postop-erative analgesia and side effects in the upper-abdominal surgery and hip replacement surgery,and ex-plore the potential mechanisms.Methods One hundred patients scheduled for selective upper-abdomi-nal operation and hip replacement surgery were randomly divided into group dezocine (group D), dezocine 0.3 mg/kg combined with sufentanil 1 μg/kg group(group DS1),dezocine 0.3 mg/kg com-bined with sufentanil 1.5 μg/kg group(group DS2)and dezocine 0.3 mg/kg combined with sufentanil 2 μg/kg group(group DS3).Analgesia was maintained by remifentanil 6-8 μg·kg-1·h-1 under total intravenous anesthesia.Patients were administered 5 μg sufentanil during sewing the skin.Visual Analogue Score (VAS)of both silence and 90°turn over situation,Ramsay score,and adverse effects at 1 h (T1 ),4 h (T2 ),8 h (T3 ),12 h (T4 ),24 h (T5 ),36 h (T6 ),48 h (T7 )after the operation were recorded respectively.Results The total amount of sufentanil and dezocine of group DS1 group showed a significant higher than the other three groups (P <0.05).The VAS in silence of group DS1 were higher than group DS3 at T1-T3 (P <0.05).There was no significant difference in VAS under 90°turn over situation.The side effect of group DS3 were higher than the other three groups (P <0.05).Conclusion Dezocine combined with sufentanil for postoperative patient-controlled intravenous analgesia(PCIA)is effective and safe in patients undergoing upper-abdominal surgery and hip replace-ment surgery,and while dezocine 0.3 mg/kg combined with sufentanil 1.5 μg/kg,it has the best effect of postoperative analgesia and least side effects.