Objective To investigate the effects of endaravane on hypoxia-ischemia (HI)-induced brain injury in neonatal piglets. Methods Male piglets 3-7 days old weighing 2.0-3.0 kg were used in this study. Group Ⅰ 10 piglets were randomly collected as sham operation without HI. Twenty piglets with HI were randomly divided into 2 groups (n = 10 each) : group Ⅱ HI and group Ⅲ HI + endaravone. The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg, tracheostomized and mechanically ventilated with 30% O_2. Right femoral artery and vein were cannulated. MAP, HR, PET CO_2, blood gases and glucose and rectal temperature were monitored. After 15 min stabilization cardiac arrest was induced by inhalation of hypoxic air (O_2 10%) for 40 min followed by inhalation of 21% O_2 for 5 min. The tracheal tube was then occluded for 7 min. Cardio-pulmonary resuscitation (CPR) was then started until recovery of spontaneous circulation (ROSC). CPR > 3 min was considered a failure. A bolus of endaravone 3 mg/kg was given iv over an hour at 30 min after CPR,followed by continuous infusion at 1.5 mg·kg~(-1)·h~(-1) for 5.5 h in group Ⅲ , while in group Ⅱ vehicle was given instead of endaravone. The neurological function of the animals was evaluated at 48, 72 and 96 h after ROSC and scored (0-154, 0 = normal, 154 = severest dysfunction). The animals were killed at 96 h after ROSC. The brains were removed for microscopic examination of striatum and cortex and determination of 8-hydroxy-2'-deoxyguanine (8-OHdG/OHG) expression in putamen by immuno-histochemistry. Results The neurological function scores were significantly higher at 48 h after ROSC and the number of viable neurons in striatum and sensory cortex were significantly lower and the expression of 8-OHdG/OHG in putamen was significantly higher in group Ⅱ than in group Ⅲ . Conclusion The antioxidant endaravone given after CPR can attenuate Hl-induced brain injury by inhibiting oxidative damage to DNA and RNA.

Objective To investigate the effects of midazolam on hypoxic-ischemic (HI) brain injury in neonatal piglets.Methods Twenty-four newborn male piglets 3-7 days old weighing 1.8-3,0 kg were randomly divided into 3 groups ( n = 8 each): sham group (group S), HI + normal saline group (group HI-S) and HI + midasolam group (group HI-M). The animals of group HI-S and HI-M were subjected to 7 min of hypoxia, producing asphyxic cardiac arrest, followed by cardiopulmonary resuscitation. At 3 h after restoration of spontaneous circulation (ROSC), animals received i.v. infusion of fentanyl at a rate of 10-30 μg·kg-1·h-1 and pancuroniumat a rate of 0.1-0.2 mg·kg-1·h-1 from 3 h after ROSC to 24 h after ROSC to maintain the anesthesia. In addition, midazolam at a rate of 0.05 mg·kg-1·h-1 wee infused simultaneously until 24 h after ROSC in HI-M group, while the equal volume of normal saline was infused instead in group HI-S and S. Arterial blood samples were taken before hypoxia (baseline), and at 37 min of hypoxia, 5 min of air inspiration, 5 min of asphyxia and 6, 12, and 24 h after ROSC for blood gas analysis, and MAP was monitored at the each time point. Neurological behavior was assessed and scored (NBS) at 48, 72, 96 and 240 h after ROSC. Brains were removed at 10 h after ROSC, the remaining viable neurons in putamen and candate nucleus were counted and the density of viable neurons was determined using light microscopic examination. Results PaO2 was significantly decreased during hypoxia-eephyxia, and PaCO2 was significantly increased, while pH value and MAP were significantly decreased at 5 min of asphyxia in group HI-S and HI-M compared with group S and the baseline (P < 0.05).There were no significant differences in MAP and arterial blood gas analysis at the each time point between group HI-S and HI-M ( P > 0.05). The density of viable neurons in putamen and caudate nucleus was significantly lower, and NBS at 48-96 h after BOSC significantly higher in group HI-S and HI-M than in group S ( P < 0.05). The density of viable neurons in putamen and caudate nucleus was significantly higher and NBS at 72 and 96 h after ROSC significantly lower in group HI-M than in group HI-S ( P < 0.05). Conclusion Midazolam used at the early stage of cardiopulmonary resuscitation can attenuate HI brain injury in neonatal piglets.

Objective To evaluate the efficacy of continuous stellate ganglion block (SGB) for prevention of cerebral vasospasm (CVS) following interventional treatment of intracranial aneurysms.Methods Forty patients of both sexes with ruptured intracranial aneurysm,aged 20-60 yr,of American Society of Anesthesiologists physical status Ⅱ or Ⅲ,with Hunt-Hess grade Ⅰ-Ⅲ,scheduled for elective interventional treatment of intracranial aneurysms,were divided into 2 groups (n =20 each) using a random number table:control group (C group) and continuous SGB group (SGB group).After induction of anesthesia,patients received ipsilateral continuous SGB with 0.25％ ropivacaine 6-8 ml followed by continuous infusion of 0.2％ ropivacaine 2 ml/h for 3 days in group SGB.Transcranial Doppler ultrasound was used to measure the blood flow in bilateral middle cerebral arteries and internal carotid arteries within 3 days after operation,and the development of CVS was assessed.Before operation and at 2 and 6 h and 1 and 3 days after operation,blood samples were collected from the internal jugular vein for determination of plasma melatonin (MT) and endothelin-1 (ET-1) concentrations by enzyme-linked immunosorbent assay.Results Compared with group C,the incidence of CVS (5％) was significantly decreased,and the plasma ET-1 concentration was decreased at 2 and 6 h and 1 and 3 days after operation (P ＜ 0.05),and no significant change was found in plasma MT concentrations at each time point in group SGB (P＞0.05).Conclusion Continuous SGB can effectively prevent the development of CVS following interventional treatment of intracranial aneurysms,and the mechanism may be related to inhibited release of ET-1 from vascular endothelial cells,but not related to MT.

Objective To evaluate the relationship between emergence agitation (EA) during recovery from general anesthesia and postoperative cognitive dysfunction (POCD).Methods Two hundred and eighty ASA Ⅰ or Ⅱ patients,aged 18-70 yr,weighing 52-80 kg,undergoing elective surgery,were included.Anesthesia was induced with midazolam,fentanyl,propofol and cisatracurium.The patients were tracheal intubated and mechanically ventilated.Anesthesia was maintained with remifentanil,propofol and cisatracurium.EA was assessed at 15-40 min after extubation by using Post-operative Quality Recovery Scale and the cognitive function was assessed at day 1 before operation and days 1-7 after operation.Patients were divided into POCD or nonPOCD group according to the occurrence of POCD.The general data of patients,preoperative complications and types of surgery were recorded.If there was significant difference between the 2 groups,the factor was analyzed using multi-factor logistic regression to select the risk factor for incidence of POCD.Results The incidence of POCD was 40.7 ％.The results of logistic regression analysis showed that the dangerous degree of the risk factors for POCD in order from high to low were emergence agitation,duration of anesthesia and age.Conclusion EA during recovery from general anesthesia is an independent risk factor for POCD.

Objective To investigate the effects of a single exposure or multiple exposures with equivalent total duration of exposure to sevoflurane on the histological morphology and neurons ultrastructure changes in neonatal rats hippocampus CA1.Methods A total of 45 male Sprague-Dawley rats on postnatal day 7,weighing 14-18 g,were randomly divided into three groups (n=15 each): Control group (group C),single exposure to sevoflurane group (group SS),multiple exposures to sevoflurane group (group TS).In group SS,the rats inhaled 3% sevoflurane for 6 h on postnatal day 7.In group TS,the rats inhaled 3% sevoflurane for 2 h on postnatal day 7,8 and 9.In group C,the rats inhaled 60% oxygen on the corresponding day age.Rats were sacrificed and brain were seperated on postnatal day 14.CA1 pyramidal neurons pathological morphology and quantity changes were observed by Hematoxylin-Eosin (HE) and Nissl staining.In the meantime,transmission electron microscopy was used for observing neurons ultrastructure and measuring the thickness of the postsynaptic density and the length of the postsynaptic active area.Results Nissl staining and HE indicated that multiple exposures and a single 6 h exposure to sevoflurane resulted in severer neurons loss and sparse arrangement relative to group C (P<0.05),Multiple exposures to sevoflurane resulted in greater neurons loss compared with a single 6-h exposure (P<0.05).Transmission electron microscope indicated that damage of CA1 neuronal subcellular organelle induced by multiple exposures and a single 6 h exposure was severer compared with group C.Both multiple exposures and a single exposure lead to decreased thickness of the postsynaptic density and shorter length of the postsynaptic active area (P<0.05).Multiple exposures to sevoflurane caused greater damaged than a single exposure (P<0.05).Conclusion Both a single and multiple exposure to sevoflurane induced CA1 neurons loss and ultrastructure changes in neonatal rats.Compared with a single exposure,multiple exposures to sevoflurane resulted in greater neurons morphology injury.

Objective To observe the analgesia effects of ropivacaine with sufentanil or dezocine on continuous femoral nerve block (FNB)after total knee arthroplasty (TKA).Methods Sixty un-dergoing selective unilateral TKA patients,received postoperative analgesia with continuous FNB for 48 hours,were randomly divided into three groups according to the drug formulations:0.225% ropiv-acaine (group R),0.1 5% ropivacaine mixed dezocine 10 mg (group D),and 0.1 5% ropivacaine mixed sufentanil 1 μg/kg (group S);the visual analogue scale (VAS)in resting state (RVAS), active functional exercise state (AVAS),passive functional exercise state (PVAS)were recorded at 1,3,7 d after surgery.The other analgesics dosage and the incidence of nausea and vomiting and other complications were recorded.Results Compared with preoperative state,the RVAS scores in three groups were significantly lower at 1,3,7 d after surgery,the PVAS scores were significantly lower at 7 d after surgery (P <0.05).Compared with group R,the RVAS scores were significantly higher ei-ther in groups S or D at the 3 d postoperatively (P <0.05).There were no significantly difference in adverse reaction among three groups.Conclusion Ropivacaine combined with sufentanil or dezocine through continuous FNB can provide a effectual postoperative analgesia in TKA patients without an increase in adverse events.But compared to 0.225% ropivacaine,0.1 5% ropivacaine with sufentanil or dezocine may not keep a longer analgesia duration,this is more obvious observed in dezocine group.

Objective To investigate the effects of remifentanil on lipid peroxidation druing hemorrhagic shock-induced acute lung injury (ALI) in rabbits. Methods Thirty-two healthy adult rabbits weighing 2.0-2.5 kg were randomly divided into 4 groups (n = 8 each): sham operation group (group S); ALI group; low-dose remifentanil group (group LR); high-dose remifentanil group (group HR). The left femoral artery was cannulated for blood-letting and blood sampling. The right femoral artery was cannulated for remifentanil administration. The model of hemorrhagic shock was established by modified Wigger' s methods. In group S, only cannulation was performed. In group LR and HR, remifentanil was infused intraperitoneally at 0.66 and 1.32 μg·kg-1 ·min-1 15 min before blood-letting respectively, while group ALI received equal volume of normal saline instead. Arterial blood samples were taken at 0, 20,70 and 100 min after blood-letting (T1-4) for blood gas analysis. The animals were then sacrificed and the lungs were immediately removed for histological examination with light microscope and determination of W/D lung weight ratio, MDA content and SOD activity. Results W/D ratio and MDA content were significantly increased, while SOD activity was significantly decreased in group ALI compared with group S (P ＜0.05). The pH value at T2 and PaO2 at T2-4 in group LR and the pH value and PaCO2 at T2-4 in group HR were significantly higher than those in group ALI (P ＜ 0.05). W/D ratio and MDA content were significantly lower,while SOD activity was significantly higher in group LR and HR than in group ALI, and in group HR than in group LR (P ＜ 0.05). Remifentanil infusion significantly attenuated the pathologic changes in a dose-dependent manner. Conclusion Remifentanil pretreatment can attenuate hemorrhagic shock-induced ALI through inhibiting lipid peroxidation in rabbits.

Objective To evaluate the remission situation of early re-induction with priming low dose regimen containing G-CSF in treating acute myeloid leukemia (AML).Methods Ninety-seven AML patients in our hospital from March 2015 to January 2017 were retrospectively analyzed.All cases adopted the standard DA regimen for conducting the induction chemotherapy,among them,38 cases had significant residual disease on 14 d of induction chemotherapy,21 cases adopted the low dose priming regimen for conducting the early re-induction chemotherapy,17 cases adopted the tandard DA gregimen for conducting the re-induction chemotherapy.The complete remission(CR) rate and and adverse reactions were compared between two groups.Results The total CR rate in all 97 cases was 60.8％;among 38 cases needing re-induction chemotherapy,the CR rate in the priming regimen re-induction group was 76.2 ％,which was significantly higher than 41.2 ％ in the DA regimen re-induction group,the difference was statistically significant (P=0.028);the occurrence rates of side effects such as infection and cytopenia during re-induction chemotherapy process had no difference between two groups(P＞0.05).Conclusion For AML patients with obvious residual disease on 14 d of induction chemotherapy,adopting low dose priming regimen in re-duction chemotherapy has higher CR,which is superior to the standard DA regimen.

Objective To evaluate the effect of Iduna protein overexpression on poly(ADP-ribose) polymerase 1 ( PARP-1)∕apoptosis-inducing factor ( AIF) pathway during oxygen-glucose deprivation (OGD)-induced damage to hippocampal neurons in neonatal rats. Methods Primarily cultured hippocam-pal neurons of healthy Sprague-Dawley rats born within 24 h were isolated and cultured. Hippocampal neu-rons were divided into 4 groups (n = 40 each) using a random number table: control group (group C), OGD group ( group O), negative control lentivirus group ( group NL) and Iduna protein overexpression group (group IO). OGD was induced by incubating the neurons in glucose-free medium and hypoxic envi-ronment. Negative control lentivirus and recombinant lentivirus overexpressing Iduna were added at 48 h be-fore establishing the model in NL and IO groups, respectively. Neurons were cultured in the normal culture medium for 24 h in group C. The cell survival rate was detected using methyl thiazolyl tetrazolium assay, the lactic dehydrogenase (LDH) leakage rate was measured using colorimetric method, the comet assay was used to detect DNA content in the tail of neurons, and the expression of PARP-1, cytochrome C (Cyt c) and AIF in the nucleus was detecteded by Western blot. Results Compared with group C, the survival rate of neurons was significantly decreased, the LDH leakage rate and DNA content in the tail of neurons were increased, and the expression of PARP-1, Cyt c and AIF was up-regulated in the other three groups (P<0. 05). Compared with group O, the survival rate of neurons was significantly increased, the LDH leakage rate and the DNA content in the tail of neurons was decreased, and the expression of PARP-1, Cyt c and AIF was down-regulated in group IO (P<0. 05), and no significant change was found in group NL (P>0. 05). Compared with the group NL, the survival rate of neurons was significantly increased, and the LDH leakage rate and DNA content in the tail of neurons were decreased, and the expression of PARP-1, AIF and Cyt c was down-regulated in the group IO (P<0. 05). Conclusion Iduna protein overexpression reduces OGD-induced damage to hippocampal neurons through inhibiting PARP-1∕AIF pathway in neonatal rats.

Objective To investigate the role of orexin-A in doxapram-induced promotion of emergence from general anesthesia in patients.Methods Forty-four patients of both sexes,aged 18-60 yr,with body mass index of 21-25 kg/m2,of American Society of Anesthesiology physical status Ⅰ or Ⅱ,scheduled for elective lumbar surgery under general anesthesia,were divided into 2 groups (n =22 each) using a random number table:control group and doxapram group.Anesthesia was induced by intravenously injecting propofol,sufentanil and cisatracurium.The patients were mechanically ventilated after tracheal intubation.Anesthesia was maintained by inhaling sevoflurane and target-controlled infusion of remifentanil.Sevoflurane inhalation and remifentanil infusion were stopped at the end of operation,oxygen flow rate was adjusted to 6 L/min,doxapram 0.5 mg/kg were intravenously injected at the same time in doxapram group,and the equal volume of normal saline was given in control group.The emergence time and extubation time were recorded.On admission to operating room (T0),at 1 h after anesthesia induction (T1) and 5 and 30 min after tracheal extubation (T2,3),arterial blood samples were collected for determination of blood glucose concentrations and plasma orexin-A concentrations (by radioimmunoassay).Results Compared with the baseline at T0,blood glucose concentrations were significantly decreased at T1 and increased at T3,and plasma orexin-A concentrations were increased at T2 in two groups (P ＜ 0.05).Compared with control group,the time to eye opening and extubation time were significantly shortened,plasma orexin-A concentrations were increased at T2 (P＜0.05),and no significant change was found in blood glucose concentrations at each time point in doxapram group (P＞0.05).Conclusion The mechanism by which doxapram promotes emergence from general anesthesia may be related to increasing plasma orexin-A concentrations in patients.