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Objective:To evaluate the role of silent information regulator-1 (SIRT1)/nucleotide-binding domain (NOD)-like receptor protein-3 (NLRP3) signaling pathway in sevoflurane postconditioning-induced attenuation of oxygen-glucose deprivation and restoration (OGD/R) injury in mouse hippocampal neuronal cell line (HT22) cells.Methods:The HT22 cells were seeded in a culture plate (96-well plate, 100 μl/well; 6-well plate, 2 ml/well) at the density of 5×10 4 cells/ml or in a culture dish (6 cm in diameter) and then divided into 4 groups ( n=24 each) using a random number table method: control group (Control group), OGD/R group, sevoflurane postconditioning group (SPC group), and SIRT1 small interfering RNA group (si-SIRT 1 group). In Control group, cells were cultured at 37 ℃ in normal culture atmosphere. In OGD/R group, the culture medium was replaced with glucose-free serum-free culture medium, and cells were exposed to 95% N 2+ 5% CO 2 for 4 h in an incubator at 37 ℃, and then the glucose-free serum-free culture medium was replaced with the primary culture medium, and cells were cultured for 24 h at 37 ℃ in normal culture atmosphere. In SPC group, the glucose-free serum-free culture medium was replaced with the primary cell culture medium after 4-h oxygen and glucose deprivation, the cells were put into the hypoxia incubator chamber which was filled with 2% sevoflurane immediately after start of reoxygenation, then the chamber was placed in an incubator and the cells were cultured for 1 h at 37 ℃ in normal culture atmosphere, and finally the cells were removed from the chamber and cultured for 23 h at 37 ℃ in normal culture atmosphere. In si-SIRT1 group, SIRT1 small interfering RNA 150 pmol was added at 24 h before surgery, cells were then incubated, and the other procedures were the same as those previously described in group SPC. The cell survival rate was determined using MTT assay. TUNEL assay was used to detect cell apoptosis, and the apoptosis rate was calculated. The expression of SIRT1, NLRP3, IL-1β and IL-18 mRNA was determined using polymerase chain reaction. The expression of SIRT1, NLRP3, interleukin-1beta (IL-1β) and IL-18 was detected using Western blot. Results:Compared with Control group, the cell survival rate was significantly decreased, the apoptosis rate was increased, the expression of SIRT1 protein and mRNA was down-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was up-regulated in OGD/R group ( P<0.05). Compared with OGD/R group, the cell survival rate was significantly increased, the apoptosis rate was decreased, the expression of SIRT1 protein and mRNA was up-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was down-regulated in SPC group ( P<0.05). Compared with SPC group, the cell survival rate was significantly decreased, the apoptosis rate was increased, the expression of SIRT1 protein and mRNA was down-regulated, and the expression of NLRP3, IL-1β and IL-18 protein and mRNA was up-regulated in si-SIRT1 group ( P<0.05). Conclusions:Activation of SIRT1-NLRP3 signaling pathway is involved in sevoflurane postconditioning-induced attenuation of OGD/R injury in HT22 cells.
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Objective To evaluate the treatment effect of combination of dexmedetomidine and droperidol on emergence agitation during general anesthesia recovery period in the elderly undergoing thoracotomy. Methods Sixty patients with severe emergence agitation during general anesthesia recovery period undergoing thoracotomy for esophageal cancer or pulmonary lobectomy, aged 66-75 years, falling into ASA physical status Ⅱ or Ⅲ, were divided into three groups, 20 patients in each according to table of random number: group droperidol (group F) and group dexmedetomidine (group D) and group dexmedetomidine combining droperidol (group DF). In group F, 0.06 mg/kg droperidol was administrated via central vein. In group D, 1 μg/kg dexmedetomidine was pumped via central vein in 10 min, followed by continuous infusion of dexmedetomidine in 0.2 μg·kg-1·h-1 for 1 h. While in group DF, 0.03 mg/kg droperidol was administrated via central vein and 0.5 μg/kg dexmedetomidine was pumped via central vein in 10 min, then followed by continuous infusion of dexmedetomidine in 0.2 μg·kg-1·h-1 for 1 h. The agitation scores and the Ramsay scores were collected after the beginning of anti-agitation. Arterial blood partial pressure of carbon dioxide was tested. Postoperative complications including nausea and vomiting were recorded. Results Compared with group D, the agitation scores at 5, 10, 15 and 20 min in group DF were lower (P ＜ 0.05). Comparing with group F, the agitation scores at 60, 90 and 120 min in group DF were lower (P ＜ 0.05). The incidence of over-sedation in group DF and in group D was less than that in group F (P ＜ 0.05). PaCO2 was unaltered in all the groups after treatment. The incidence of nausea, vomiting, bradycardia, hypertension, hypotension and respiration depression and long QT interval between the groups were comparable. Conclusion Combination of dexmedetomidine and droperidol is effective and safe in the treatment of agitation during sevoflurane general anesthesia recovery period in the elderly undergoing thoracotomy.
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Objective To evaluate the role of mitochondrial permeability transition pore (mPTP)in reduction of brain injury by sevoflurane postconditioning in a rat model of hemorrhagic shock and resuscitation (HSR).Methods Ninety pathogen-free healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 5 groups (n =18 each) using a random number table:sham operation group (group S),group HSR,sevoflurane postconditioning group (group SP),sevoflurane postconditioning plus atractyloside (ATR,a specific mPTP opener) group (group SP + ATR) and ATR group.Hemorrhagic shock was produced by withdrawing 40％ of the total blood volume from the right carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated by infusion of the shed blood via the left jugular vein over 30 min.SP and SP+ATR groups were exposed to 2.4％ sevoflurane for 30 min starting from the onset of reinfusion.In ATR and SP+ATR groups,ATR 5 mg/kg was intravenously injected at 10 min before reinfusion.Six rats in each group were randomly sacrificed at 24 h after the end of autologous blood reinfusion,and the hippocampus was harvested for determination of the expression of Bcl-2 and Bax in hippocampal tissues (by Western blot) and degree of mPTP opening.At 72 h after the end of autologous blood reinfusion,the rest 6 rats in each group were selected and underwent Morris water maze test,and the cognitive function was evaluated.Results Compared with group S,the escape latency was significantly prolonged,the number of crossing the original platform and locomotor distance in the target quadrant were decreased,the expression of Bcl-2 was down-regulated,the expression of Bax was up-regulated,and the degree of mPTP opening was increased in group HSR (P＜0.05).Compared with group HSR,the escape latency was significantly shortened,the number of crossing the original platform and locomotor distance in the target quadrant were increased,the expression of Bcl-2 was up-regulated,the expression of Bax was down-regulated,and the degree of mPTP opening was decreased in group SP (P＜0.05),and no significant change was found in each parameter in ATR and SP+ATR groups (P＞0.05).Compared with group SP,the escape latency was significantly prolonged,the number of crossing the original platform and locomotor distance in the target quadrant were decreased,the expression of Bcl-2 was down-regulated,the expression of Bax was up-regulated,and the degree of mPTP opening was increased in group SP+ATR (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning ameliorates brain injury may be related to inhibiting mPTP opening in a rat model of HSR.
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Objective To evalute the role of phosphatidylinositol 3?kinase(PI3K)∕serine?threo?nine kinase(Akt)∕endothelial nitric oxide synthase(eNOS)signaling pathway in sevoflurane postcondi?tioning?induced attenuation of brain injury in a rat model of hemorrhagic shock and resuscitation(HSR). Methods Seventy?two pathogen?free healthy adult male Sprague?Dawleg rats, weighing 300-350 g, were divided into 4 groups(n=18 each)using a random number table: sham operation group(group S), group HSR, sevoflurane postconditioning group(group SP)and sevoflurane postconditioning plus PI3K∕Akt signaling pathway specific inhibitor wortmannin group(group SP+WT). Hemorrhagic shock was in?duced by withdrawing blood(40% of the total blood volume)from the right common carotid artery over an interval of 30 min, and 1 h later the animals were resuscitated with infusion of the shed blood via the left jugular vein over 30 min. In group SP+WT, wortmannin 0.6 mg∕kg was administrated via the jugular vein at 30 min before establishment of the model. In SP and SP+WT groups, 2.4% sevoflurane was inhaled for 30 min starting from the onset of infusion of the shed blood. At 10 min before withdrawing blood(T0), im?mediately after the end of withdrawing blood(T1), at 30 min and 1 h after the end of withdrawing blood (T2,3)and immediately after infusion of the shed blood(T4), blood samples from the common carotid ar?tery were collected for blood gas analysis, the blood lactate concentration was recorded, and mean arterial pressure was simultaneously recorded. At 24 h after infusion of the shed blood, 6 rats were randomly select?ed from each group and sacrificed, and their brains were immediately removed for determination of cerebral infarct volume(by TTC staining), expression of hippocampal caspase?3(by immuno?histochemistry), and expression of Akt, phosphorylated Akt(p?Akt)and eNOS(by Western blot). The ratio of p?Akt∕Akt was calculated. Results Compared with group S, the mean arterial pressure was significantly decreased and the blood lactate concentration was increased at T1?3, the cerebral infarct volume was increased, and the expression of caspase?3 was up?regulated in the other three groups, and the ratio of p?Akt∕Akt was sig?nificantly increased, and eNOS expression was up?regulated in group SP(P<0.05). Compared with group HSR, the cerebral infarct volume was significantly decreased, the expression of caspase?3 was down?regula?ted, the ratio of p?Akt∕Akt was increased, and eNOS expression was up?regulated in group SP(P<0.05). Compared with group SP, the cerebral infarct volume was significantly increased, the expression of caspase?3 was up?regulated, the ratio of p?Akt∕Akt was decreased, and eNOS expression was down?regula?ted in group SP+WT(P<0.05). Conclusion PI3K∕Akt∕eNOS signaling pathway activation mediates sevoflurane postconditioning?induced attenuation of brain injury in a rat model of HSR.
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Objective To evaluate the effect of sevoflurane postconditioning on inositol-requiring enzyme 1 (IRE1) signaling pathway in the brain tissues in a rat model of hemorrhagic shock and resuscitation (HSR).Methods Sixty healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 5 groups (n =12 each) using a random number table:sham operation group (group Sham),group HSR,1.2％ sevoflurane postconditioning group (group SP1),2.4％ sevoflurane postconditioning group (group SP2) and 3.6％ sevoflurane postconditioning group (group SP3).Hemorrhagic shock was induced by withdrawing blood (40％ of the total blood volume) from the right common carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated with the shed blood infused via the left jugular vein over 30 min.SP1,SP2 and SP3 groups inhaled 1.2％,2.4％ and 3.6％ sevoflurane,respectively,for 30 min starting from the beginning of infusion of the shed blood.Oxygen was inhaled for 30 min instead of sevoflurane in Sham and HSR groups.Mean arterial pressure was recorded before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),at 30 min after the end of withdrawing blood (T2),before infusion of the shed blood (T3),and immediately after infusion of the shed blood (T4).Arterial blood samples were obtained at T0,T1,T3 and T4 for blood gas analysis.Morris water maze test was performed at 72 h after the end of infusion of the shed blood.The animals were then sacrificed,and brains were removed for determination of the expression of caspase-3 in hippocampal CA1 region (by immunohistochemistry) and expression of IRE1 and X-box binding protein 1 (XBP1) in hippocampal tissues (by Western blot).Results Compared with group Sham,mean arterial pressure was significantly decreased at T1-3,the pH value and base excess were decreased,lactic acid concentrations were increased,the escape latency was prolonged,the frequency of crossing the original platform was decreased,and the expression of caspase-3 in hippocampal CA1 regitn and IRE1 and X BP 1 in hippocampal tissues was up-reg ulated in group HSR (P＜0.05).Compared with group HSR,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and the expression of caspase-3 in hippocampal CA1 region and IRE1 and XBP1 in hippocampal tissues was down-regulated in SP2 and SP3 groups (P＜0.05),and no significant changes were found in the parameters mentioned above in group SP1 (P＞0.05).Conclusion The mechanism by which sevoflurane postconditioning reduces brain injury may be related to activating IRE1 signaling pathway in the brain tissues in a rat model of HSR.
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Objective To evaluate the efficacy of pressure-controlled volume-guaranteed (PCVVG) mode for lung protective ventilation in patients requiring one-lung ventilation (OLV) during thoracoscopic surgery.Methods Sixty patients,aged 50-70 yr,with body mass index of 18-26 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective radical resection of esophageal cancer performed via video-assisted thoracoscope under general anesthesia,were divided into 2 groups (n=30 each) using a random number table:volume-controlled ventilation group (group V) and PCV-VG group (group P).The ventilator settings were adjusted,with a tidal volume 10 ml/kg and respiratory rate 10-12 breaths/min during two-lung ventilation,and with a tidal volume 6 ml/kg and respiratory rate 12-16 breaths/min during OLV.The inspiratory/expiratory ratio was 1 ∶ 2,pressure restriction was 35 cmH2O,and 33％ oxygen was inhaled at 2 L/min.The end-tidal pressure of carbon dioxide was maintained at 35-40 mmHg.Visual analog scale score was maintained ≤ 3 after operation.After admission to the operation room (T0) and at 1,3 and 7 days after operation (T1-3),forced vital capacity (FVC),forced expiratory volume in first second (FEV1),and maximal mid-expiratory flow (MMEF) were measured,arterial blood samples were collected for blood gas analysis,arterial carbon dioxide partial pressure and arterial oxygen partial pressure (PaO2) were recorded,and alveolar-arterial oxygen tension difference (PA-a O2) was calculated.Clinical Pulmonary Infection Score was assessed at T1,T2 and T3.The chest tube removal time and length of postoperative hospital stay were recorded.Results Compared with the baseline at T0,FVC,FEV1,MMEF and PaO2 were significantly decreased,and PA-aO2 was increased at T1-3 in the two groups (P＜0.05).Compared with group V,FVC,FEV1,MMEF and PaO2 were significantly increased,PA-aO2 and Clinical Pulmonary Infection Score were decreased,and the chest tube removal time and length of postoperative hospital stay were shortened at T1-3 in group P (P＜0.05).Conclusion PCV-VG mode can achieve lung protective ventilation,which is helpful in improving outcomes in the patients requiring OLV during thoracoscopic surgery.
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Objective To evaluate the effect of sevoflurane postconditioning on the expression of CCAAT/enhancer-binding protein homologous protein (CHOP) in a rat model of hemorrhagic shock and resuscitation.Methods Thirty-six healthy adult male Sprague-Dawley rats,weighing 300-350 g,were divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),hemorrhagic shock and resuscitation group (group HSR) and sevoflurane postconditioning group (group SP).Hemorrhagic shock was induced by withdrawing 40% of the total blood volume from the right carotid artery over an interval of 30 min,and 1 h later the removed blood was reinfused via the left jugular vein for resuscitation.Group SP inhaled 2.4% sevoflurane for 30 min starting from the onset of reinfusion.Mean arterial pressure was monitored and recorded at a 10 min interval.Before withdrawing blood (T0),immediately after the end of withdrawing blood(T1), at 1 h after the end of withdrawing blood(T2) and immediately after the end of reinfusion (T3),blood samples were collected from the common carotid artery for blood gas analysis.At 4 days after reinfusion,6 rats of each group were selected to detect spatial learning and memory ability by using Morris water maze test.The animals were then sacrificed,brains were removed for determination of neuronal apoptosis in hippocampal CA1 area using TUNEL.The rest 6 rats in each group were sacrificed at 72 h after reinfusion,and the hippocampus was isolated to detect the expression of CHOP by Western blot.Results Compared with group S,mean arterial pressure was significantly decreased,and lactic acid concentrations were increased at T1,2 in HSR and SP groups,and the escape latency was significantly prolonged,the percentage of time staying at the target quadrant was decreased,the number of apoptotic neurons in hippocampal CA1 area was increased,and the expression of CHOP was up-regulated in group HSR (P<0.05).Compared with group HSR,the escape latency was significantly shortened,the percentage of time staying at the target quadrant was increased,the number of apoptotic neurons in hippocampal CA1 area was decreased,and the expression of CHOP was down-regulated in group SP (P<0.05).Conclusion The mechanism by which sevoflurane postconditioning improves cognitive function is related to down-regulation of CHOP expression and inhibition of apoptosis in hippocampal neurons in a rat model of hemorrhagic shock and resuscitation.
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Objective To observe the effects of pressure control ventilation with volume guar-antee (PCV-VG)on the pulmonary function during percutaneous nephrolithotomy procedures in pa-tients with general anesthesia.Methods Forty patients scheduled for percutaneous nephrolithotomy were selected and randomly allocated into PCV-VG group (n =20)and volume controlled ventilation (VCV)group (n =20).For two modes of ventilation,the goal tidal volume was 6-8 ml/kg,and the respiratory rate was contralled to 12-20 bpm.PA-a O 2 ,OI,RI,Ppk,Pmean,Cst,Hct,Lac were re-corded at intubation (T0 ),1 5 min (T1 ),30 min (T2 ),60 min (T3 ),and 120 min (L4 )after intuba-tion.Results PCV-VG resulted in significantly lower PA-a O 2 ,RI,Ppk,Pmean compared with VC ventilation (P < 0.05 or P < 0.01 ),and significantly higher OI,Cst versus VC ventilation (P <0.05 or P < 0.01).Conclusion In general anesthesia patients undergoing percutaneous nephrolithoto-my,PCV-VG is superior to VCV in terms of lower airway pressure and more stable hemodynamics, thus protects pulmonary function.
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Objective To evaluate the effect of conventional or goal-directed fluid management on hemodynamics in patients undergoing orthopaedic arthroscopic shoulder surgery in beach chair po-sition.Methods Thirty healthy adult patients,male 1 7 cases,female 13 cases,aged 18-65 years, weight 49-68 kg,ASA Ⅰor Ⅱ,undergoing elective arthroscopic shoulder surgery,were enrolled.Pa-tients were randomly assigned to the group R(Routine group,n = 1 5 )and the group S(SVV/CI/MAP-directed,n =1 5).All patients received 10 ml/kg of hydroxyethyl starch rapidly in group R;while in group S,if SVV > 13%,patients would receive 3 ml/kg of hydroxyethyl starch in 5 min, then the changes of each index were observed;if SVV 2.5 L·min-1 ·m-2 .At 5 min after anesthesia induc-tion,patients were placed in a 60° upright position.The hemodynamic changes were monitored by FloTrac/Vigileo system.Heart rate (HR),mean artery pressure(MAP),cardiac index(CI),stroke volume variation(SVV),stroke volume index (SVI),were recorded on pre-induction (T1 ),post-induc-tion (T2 ),immediately after in beach chair position (T3 ),5 min after in beach chair position(T4 ),30 min after in beach chair position(T5 ),and at the end of surgery(T6 ).The duration of surgery,crys-talloid requirements,colloid requirements,urinary output,the dose of vasoactive drugs and the inci-dence of hypotension were recorded.Results Compared with T1 ,MAP,CI and SVI at T3-T5 point (after in BCP to the end of the surgery)were higher in both group(P <0.05 ).Compared with T2 , SVV in group R at T3-T5 were significantly increased (P <0.05),while SVV in group S only at T3 was slightly increased (P <0.05).Compared with group R,MAP,CI and SVI at T3-T5 were signif-icantly higher respectively,while SVV were higher at T3-T5 in group R (P <0.05).Compared with group R,the colloid requirements and total requirements in group S were significantly increased(P <0.05).Compared with group R,the doses of dopamine and ephedrine,the urinary output,the inci-dence of hypotension in group S were significantly reduced(P <0.05).Conclusion SVV/CI/MAP-di-rected fluid management is safer,more effective and renders much more stable hemodynamic than the routine fluid management.
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Objective To evaluate the effect of positive end-expiratory pressure (PEEP) on intraoperative pulmonary function in the patients undergoing urological retroperitoneal laparoscopic surgery in the mode of protective ventilation.Methods Forty patients of both sexes,aged 30-64 yr,with body mass index of 16-29 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective retroperitoneal laparoscopic ureterolithotorny,were randomly divided into 2 groups (n =20 each) using a random number table:control group (group C) and PEEP group (group P).After induction of general anesthesia,the patients were endotracheally intubated.Intermittent positive pressure ventilation (tidal volume [Vr] 6 ml/kg,respiratory rate [RR] 12 breaths/min,inspiratory/expiratory ratio [I:E] 1:2,fraction of inspired oxygen 50％) was performed from the end of intubation until the onset of pneumoperitoneum.After the onset of pneumoperitoneum,the patients were ventilated (VT 6 ml/kg,RR 22 breaths/min,I:E 1.0:1.5),and the end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg in group C.After the onset of pneumoperitoneum,the patients were ventilated (VT 6 ml/kg,RR 22 breaths/min,I:E1.0:1.5,PEEP 5 cmH2O),and the end-tidal pressure of carbon dioxide was maintained at 35-45 mmHg in group P.At 5 min before pneumoperitoneum (T1),at 10,30 and 60 min of pneumoperitoneum (T2-4),immediately after the end of pneumoperitoneum (T5),and at 5 min before extubation (T6),arterial blood samples were collected for blood gas analysis.Peak airway pressure and mean airway pressure were also recorded.Dynamic lung compliance,oxygenation index,respiratory index,dead space fraction and alveolararterial oxygen gradient were calculated.Results Compared with group C,mean airway pressure was significantly higher at T2-4,oxygenation index was significantly higher at T3,alveolar-arterial oxygen gradient difference was significantly lower at T3 and T6,and respiratory index was significantly lower at T6 (P＜0.05),and no significant change was found in the peak airway pressure,dynamic lung compliance and dead space fraction at each time point in group P (P＞0.05).Conclusion PEEP (5 cmH2O) can improve the intraoperative pulmonary function in the patients undergoing urological retroperitoneal laparoscopic surgery in the mode of protective ventilation.
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Objective To evaluate the effect of sevoflurane postconditioning on the expression of activating transcription factor 6 (ATF6) in the brain tissues in a rat model of hemorrhagic shock and resuscitation.Methods Thirty-six pathogen-free healthy adult male Sprague-Dawley rats,weighing 300-350 g,were randomized into 3 groups (n=12 each) using a random number table:sham operation group (group S);hemorrhagic shock and resuscitation group (group HSR);sevoflurane postconditioning group (group SP).Hemorrhagic shock was induced by withdrawing blood (40％ of the total blood volume) from the right common carotid artery over an interval of 30 min,and 1 h later the animals were resuscitated with infusion of the shed blood via the left jugular vein over 30 min.In group SP,2.4％ sevoflurane was inhaled for 30 min starting from the onset of infusion of the shed blood.Mean arterial pressure was recorded before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),at 30 min after the end of withdrawing blood (T2),before infusion of the shed blood (T3),and immediately after infusion of the shed blood (T4).The arterial blood samples were obtained at T0,T1,T3 and T4 for blood gas analysis.At 72 h after infusion of the shed blood,6 rats were selected from each group,and cognitive function was assessed by Y-maze test.The animals were then sacrificed,and brains were removed and sliced for determination of the expression of caspase-12 in hippocampal CA1 region by immunohistochemistry.The rest 6 rats in each group were sacrificed at 72 h after infusion of the shed blood,and the hippocampus was isolated for determination of the expression of ATF6 and caspase-12 by Western blot.Results Compared with group S,mean arterial pressure was significantly decreased at T1-3 (P＜0.05),the pH value and base excess were significantly decreased at T1.3,and the blood lactic acid was significantly increased at T1,3 in HSR and SP groups,and the number of total training was significantly increased,the rate of memory retention was significantly decreased,the expression of caspase-12 in hippocampal CA 1 region was significantly up-regulated,and the expression of ATF6 and caspase-12 in hippocampal tissues was significantly up-regulated in group HSR (P＜ 0.05).Compared with group HSR,the number of total training was significantly decreased,the rate of memory retention was significantly increased,the expression of caspase-12 in hippocampal CA1 region was significantly down-regulated,and the expression of ATF6 and caspase-12 in hippocampal tissues was significantly down-regulated in group SP (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning improves cognitive function is related to down-regulation of ATF6 expression in the brain tissues in a rat model of hemorrhagic shock and resuscitation.
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Objective To evaluate the effects of limb ischemic preconditioning on myocardial ischemiareperfusion injury in a rat model of severe hemorrhagic shock and resuscitation.Methods Twenty-four male Sprague-Dawley rats,weighing 300-350 g,were randomized into 3 groups (n =8 each) using a random number table:control group (group C); severe hemorrhagic shock and resuscitation group (HSR group); limb ischemic preconditioning group (group LIP).Hemorrhagic shock and resuscitation was induced by withdrawing blood (50％ of the total blood volume) from the left common carotid artery over an interval of 1 h,and 30 min later the animals were then resuscitated by infusion of the shed blood via the jugular vein over 30 min.Limb ischemic preconditioning was induced by 4 cycles of 5 min limb ischemia followed by 5 min reperfusion at 40 min before ischemia in LIP group.Before withdrawing blood (T0),immediately after the end of withdrawing blood (T1),before infusion of the shed blood (T2),and at 0,1 and 2 h after infusion of the shed blood (T3-5),mean artery pressure (MAP) was measured,the cardiac output (CO),left ventricular ejection fraction (LVEF) and myocardial performance index (MPI) were detected using color Vivid flow imaging,and total vessel density (TVD),perfusing vessel density (PVD),proportion of perfused vessels (PPV),microvascular flow index (MFI) of sublingual microcirculation were measured using sidestream dark-field imaging.The survival rates within 72 h after hemorrhagic shock and resuscitation were recorded.Results Compared with C group,MAP,CO,LVEF,TVD,PVD,PPV and MFI were significantly decreased and MPI was increased at T1-5 in HSR group and at T1 and T2 in LIP group (P ＜ 0.01).Compared with HSR group,MAP,CO,LVEF,TVD,PVD,PPV and MFI were significantly increased and MPI was decreased at T3-5,and the survival rate within 72 h was increased in LIP group (P ＜ 0.01).Conclusion Limb ischemic preconditioning can significantly attenuate myocardial ischemiareperfusion injury induced by severe hemorrhagic shock and resuscitation in rats and is helpful for prognosis.
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Objective To obtain highly expressing cell lines by inserting the glutamine synthetase (GS) screening system and replacing the promoter of the vector.Methods The mutation of the point BamHⅠwas induced to build a new vector pIRES2-EGFP.The marker gene GS was inserted by AseⅠ and NheⅠ, and the promoter hCMV was replaced by PacⅠand NheⅠ.The new vector pHGS1.0 and the vector pIRES2-enhanced screen fluorescein protein( EGFP)-B were inserted by the recombinant protein TEM8 ( 1-227 )-VEGFR1 domain2-IgG2 ( TV-IgG2 ) gene to analyze the advantages of the expression.Results The glutamine synsthetase is successfully inserted, the human cytomegalovirus replaced, and recombinant protein is increased 5-fold by human immunoglobulin quantification kit.Conclusion The GS system is a highly protein expressing system.
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ObjectiveTo investigate the effects of morphine preconditioning on myocardial ischemiareperfusion (I/R) injury and the expression of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2)in rats with chronic heart failure.MethodsForty-eight healthy male SD rats weighing 220-250 g were randomly divided into 6 groups ( n =8 each):control group (group C),sham operation group (group S),I/R group and preconditioning with low,median and high doses of morphine groups (groups MP1-3 ).Chronic heart failure was induced by iv edriamycin 2.0 mg/kg once a week for 6 weeks in groups S,I/R and MP1-3.Left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) were measured using ultrasound,and left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were calculated at the end of 14th day after the end of adriamycin administration.Blood samples from the carotid artery were collected after ultrasonography for determination of the plasma brain natriuretic peptide (BNP) concentration.Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion at 2 day after ultrasonography in groups I/R and MP1-3.In groups MP1-3,iv morphine 0.015,0.030 and 0.050 mg/kg were repeated 3 times at 5 min interval at 30 min before ischemia respectively,while normal saline 5 ml/kg was given in group I/R.The animals were sacrificed at the end of reperfusion in groups S,I/R and MP1-3,and the hearts were removed to measure the area at risk (AAR),infarct size (IS),and IS/AAR ratio was calculated.The p-ERK1/2 expression in myocardium was assessed by Western blot.ResultsThe LVESD and plasma BNP concentration were significantly higher,while the LVEF and LVFS lower in the other 5 groups than in group C (P ＜0.01).No myocardial infarction was found in group S.The p-ERK1/2 expression was significantly lower in groups I/R and MP1 than in group S (P ＜ 0.05).IS and IS/AAR ratio were significantly lower,and p-ERK1/2expression was significantly higher in groups MP2.3 than in group I/R ( P ＜ 0.05).There were no significant differences in IS,IS/AAR ratio and p-ERK1/2 expression between groups MP1 and I/R (P ＞ 0.05).IS and IS/AAR ratio were decreased gradually,and the p-ERK1/2 expression was up-regulated gradually in groups MP1-3 ( P ＜0.05).ConclusionMorphine preconditioning can confer cardioprotection against myocardial I/R in a dose-dependent manner in rats with chronic heart failure.Up-regulation of p-ERK1/2 expression is involved in the underlying mechamism.
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Objective To investigate the effects of remifentanil postconditioning on apoptosis in hippocampal neruons in a rat model of cerebral ischemia-reperfusion(I/R)and the mechanism involved.Methods Twentyfour male SD rats weighing 250-300 g were randomly divided into 4 groups(n = 6 each): sham operation group (group S);global cerebral I/R group(group I/R);remifentanil 0.6μg·kg- 1·min-1+global cerebral I/R group (group R1)and remifentanil 1.8μg·kg-1·min-1 + global cerebral I/R group(group R2).Global cerebral ischemia was induced by 10 min occlusion of bilateral common carotid combined with hypotension.In group R1 and R2,remifentanil at 0.6 and 1.8μg·kg-1·min-1 were infused for 5 min before ischemia respectively.The cognitive function was tested with Morris water maze and step-down tests from the day 3 to day 8 after reperfusion.When Morris water maze test was finished,rat brains were removed for HE staining and determination of the expression of caspase-3 in hippocampal CA1 region by immuno-histochemistry.Apoptosis in neurons in hippocampal CA1 region was detected by TUNEL assay.Results Compared with group S,the cognitive function was significantly decreased and the number of apopotic neurons in hippocampus CA1 region increased in group I/R,R1 and R2,and the expression of caspase-3 was up-regulated in group I/R(P＜0.05).Compared with group I/R,the cognitive function was significantly increased,the expression of caspase-3 was down-regulated,and the number of apopotic neurons in hippocampus CA1 region was significantly decreased in group R1 and R2(P＜0.05).Conclusion Remifentanil postconditioning can improve the cognitive function through down-regulating caspase-3 expression and inhibiting the apoptosis in hippocampal neruons in a rat model of cerebral I/R.
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Objective To investigate the effects of parecoxib and morphine on remifentanil-induced postoperative hyperalgesia in patients undergoing orthopedic operation. Methods Sixty ASA Ⅰ or Ⅱ patients,aged 20-62 yr, weighing 45-100 kg, undergoing orthopedic surgery, were randomly divided into 3 groups ( n = 20 each). Anesthesia was induced with midazolam, propofol, remifentanil and rocuronium. The patients were mechanically ventilated after tracheal intubation. Group Ⅰ received iv injection of morphine 0.15 mg/kg, group Ⅱ received iv injection of parecoxib 20 mg and morphine 0.075 mg/kg and group Ⅲ received iv injection of parecoxib 40 mg and morphine 0.075 mg/kg. Anesthesia was maintained with infusion of propofol and remifentanil and intermittent iv boluses of vecuronium. The emergence time, consciousness recovery time, extubation time,incidence of agitation and shivering, and VRS score at 5 min after recovery of consciousness were recorded. Pain at rest and at movement was evaluated using VAS score at 1,2, 4, 8, 12 and 24 h (T1-6) after surgery and MAP andHR were recorded simultaneously. The incidence of nausea and vomiting during 24 h after surgery was also recorded. Blood samples were taken before induction of anesthesia, at the end of operation and 24 h after operation for determination of plasma concentrations of PGE2 and TNF-α. Results There was no significant difference in emergence time, consciousness recovery time, extubation time, VRS scores, MAP, HR, incidence of agitation,shivering, nausea and vomiting among the 3 groups. Compared with group Ⅰ , VAS scores at rest at T1-2 and at movement at T1-6 were significantly increased in group Ⅱ , while VAS scores at rest and at movement decreased at T1-5 in group Ⅲ (P＜0.05). VAS scores at rest at T1-6 and at movement at T1-5 were significantly lower in group Ⅲ than in group Ⅱ (P＜ 0.05). There was no significant difference in the plasma concentrations of PGE2 and TNF-α at different time points between group Ⅰ and Ⅱ (P＞0.05). The plasma concentrations of PGE2 and TNF-α were significantly lower at the end of surgery in group Ⅲ than in group Ⅰ and Ⅱ (P＜0.05). Conclusion Preoperative iv parecoxib 40 mg and morphine 0.075 mg/kg can reduce remifentanil-induced postoperative hyperalgesia in patients undergoing orthopedic operation, and the efficacy is better than that of morphine alone.
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Objective To compare the effects of different doses of dexmedetomidine in inhibition of cardiovascular response to endotracheal intubation. Methods One hundred and twenty ASA Ⅰ or Ⅱ patients, aged 18-60 yr, weighing 45-80 kg, scheduled for upper abdominal surgery, were randomly assigned to one of 4 groups (n = 30 each): control group (group C); low, median and high doses of dexmedetomidine groups (group M1-3) .In group M1-3, 15 min before anesthesia induction, dexmedetomidine 0.25, 0.5 and 1.0 μg/kg were infused over 15 min respectively, while normal saline 15 ml was given instead of dexmedetomidine in group C. After anesthesia induction, tracheal intubation was performed when the BIS value ≤ 60 and it was maintained for 5 s. The patients were mechanically ventilated. BP and HR were recorded before infusion of dexmedetomidine (T0), before intubation (T1), immediately after intubation (T2) and at 1, 3, 5 and 10 min after intubation (T3-6). Venous blood samples were also taken at the same time to measure the plasma concentrations of epinephrine (E) and norepinephrine (NE). Results Compared with T0, HR was significantly decreased at T1 in group M1-3, BP was significantly increased at T1 in group M3, and the plasma concentrations of E and NE were significantly increased at T4-6 in group C and M1(P ＜0.05). BP and HR were significantly lower at T2, while higher at T3-5 in group C and M1than at T1 (P ＜ 0.05). BP at T1-6 was significantly higher in group M3 than in group M2 (P ＜ 0.05). Conclusion When the dose of dexmedetomidine reaches 0.5 μg/kg, it may effectively inhibit the stress reaction to noxious stimulation.