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Objective:To analyze the features of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) co-infected with other common respiratory pathogens among coronavirus disease 2019 (COVID-19) patients in Shanghai City, and to provide a reference for scientific prevention and control of COVID-19 and other respiratory infectious diseases.Methods:Descriptive epidemiological approaches were used to analyze the data of COVID-19 reported cases in Shanghai City from January 2020 to February 2021 in the information system of Chinese Disease Prevention and Control. Clinical data of the participants were collected, and their SARS-CoV-2 nucleic acid-positive respiratory specimens were collected at the time of illness onset or admission. Multiplex reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect the 22 respiratory pathogens. Independent-samples t test was used for statistical analysis. Results:Of the 272 patients with COVID-19, 15(5.5%) had co-infection of SARS-CoV-2 with other respiratory pathogens, all of which were double infection. There were three cases infected with enterovirus/rhinovirus, two of each with adenovirus, human metapneumovirus and coronavirus NL63/HKU1, and one of each with coronavirus 229E, influenza A virus H1N1, parainfluenza virus 1 and respiratory syncytial virus B. Two cases infected with Mycoplasma pneumoniae. Among the 272 COVID-19 patients, 212(77.9%) had fever, 117(43.0%) had cough, 46(16.9%) had fatigue, and 35(12.9%) had sore throat. The white blood cell count of co-infection cases was higher than that of non-co-infection cases ((6.8±1.7)×10 9/L vs (5.3±1.6)×10 9/L), and the difference was statistically significant ( t=3.09, P=0.008). Conclusions:There is a certain proportion of co-infection of SARS-CoV-2 with other respiratory pathogens among the COVID-19 cases in Shanghai City, mainly viral pathogens, especially enterovirus/rhinovirus. A rational combination of drugs was recommended to improve the cure rate. Surveillance of acute respiratory infection should be further strengthened as well.
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The awake prone position plays an important role in the treatment of hypoxemia and the improvement of respiratory distress symptoms in non-intubated patients. It is widely used in clinical practice because of its simple operation, safety, and economy. To enable clinical medical staff to scientifically and normatively implement prone position for awake patients without intubation, the committees of consensus formulation, guided by evidence-based methodology and Delphi method, conducted literature search, literature quality evaluation and evidence synthesis around seven topics, including indications and contraindications, evaluation, implementation, monitoring and safety management, termination time, complication prevention and health education of awake prone position. After two rounds of expert letter consultation, Expert consensus on implementation strategy of awake prone positioning for non-intubated patients in China (2023) was formulated, and provide guidance for clinical medical staff.
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Humans , Consensus , Prone Position , Wakefulness , China , DyspneaABSTRACT
Enteral nutrition plays an irreplaceable role in the nutritional treatment of critically ill patients. In order to help clinical medical staff to manage the common complications during the implementations of enteral nutrition for critically ill patients, the consensus writing team carried out literature retrieval, literature quality evaluation, evidence synthesis. Several topics such as diarrhea, aspiration, high gastric residual volume, abdominal distension, etc. were assessed by evidence-based methodology and Delphi method. After two rounds of expert investigations, Expert consensus on prevention and management of enteral nutrition therapy complications for critically ill patients in China (2021 edition) developed, and provided guidance for clinical medical staff.
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Objective To evaluate the effect of high-frequency oscillatory ventilation (HFOV) on lung injury in the piglets with acute respiratory distress syndrome (ARDS).Methods Twelve male piglets,aged 6-8 weeks,weighing 14-16 kg,were randomly divided into 2 groups (n=6 each) using a random number table:conventional mechanical ventilation with low tidal volume group (CMV group) and HFOV group.ARDS was induced by bilateral pulmonary lavages with isotonic saline (38 ℃),repeated every 10 min until the oxygenation index＜200 mmHg.After successful establishment of the model,CMV group was ventilated using conventional mechanical ventilation with low tidal volumes.After successful establishment of the model,HFOV group was ventilated using HFOV,lung recruitment was performed,the airway pressure was set at 25 cmH2O and maintained at this level for 30 s,and the airway pressure was then adjusted 5 cmH2O higher than that after successful establishment of the model,with bias flow 25 L/min,inspiratory time ratio 33％,frequency 8 Hz,amplitude 40-80 cmH2O,and inspiratory oxygen fraction 1.0.In both groups,carbon dioxide partial pressure was maintained between 35 and 50 mmHg.Before establishment of the model (baseline),after successful establishment of the model (T1),and at 0.5,1.0,2.0 and 4.0 h after beginning of mechanical ventilation (T2-5),blood samples were collected from the femoral artery and central vein for blood gas analysis,arterial oxygen partial pressure and carbon dioxide partial pressure were recorded,oxygen delivery index,oxygen consumption index,oxygenation index and intrapulmonary shunt were calculated,and the improvement in pulmonary function (oxygenation index ≥ 200 mmHg) was recorded.At T0,T1 and T5,venous blood samples were collected for determination of the concentrations of serum Clara cell secretory protein 16,soluble intercellular adhesion molecule-1,and high-mobility group box 1.Results Compared with CMV group,the arterial oxygen partial pressure at T35 and oxygenation index at T4.5 were significantly increased (P ＜ 0.05),and no significant change was found in the other parameters in HFOV group (P＞0.05).Conclusion Compared with conventional mechanical ventilation with low tidal volumes,although HFOV improves lung oxygenation,the degree is small in the piglets with ARDS.
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Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.
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Objective To compare the hypnotic effects of propofol administered by target-controlled infusion (TCI in daytime and nighttime,in order to explore the effect of circadian rhythm on the sedative effect of propofol.Methods Sixty-five male ASA Ⅰ or Ⅱ patients,aged 18-55 years,with the body mass index (BMI) of 18.5-24.9 kg/m2,undergoing emergency minor hand surgery were divided into two groups according to the time of the day when they received TCI of propofol:daytime group (from 07:01 to 19:00) and nighttime group (from 19:01 to 07:00).The pharmacokinetic parameters proposed by Schnider et al.which suggested the effect-site concentration (Ce) was used.Four Ces of propofol were set at 0.8,1.2,2.0 and 4.0 μg/ml,respectively.Ce was increased step by step and each Ce was maintained for 5 minutes.The level of sedation at each Ce was assessed by bispectral index (BIS) and observer's assessment of alertness/sedation (OAA/S) scores.BIS values and Ces of propofol were recorded and compared between the two groups when the patients lost consciousness (OAA/S score =2).Results There were 28 and 30 patients in daytime and nighttime groups,respectively.When Ces were 1.2 and 2.0 μg/ml,the BIS values were significantly lower in the nighttime group than in the daytime group.There was no significant difference in BIS values between the two groups when Ces were 0.8 and 4.0 μg/ml.When the patients lost consciousness (OAA/S =2),the BIS value was comparable between the two groups,but Ce was significantly lower in the nighttime group than in the daytime group.Conclusion The hypnotic effect of propofol is greater during night time than during day time.
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Objective To evaluate the effect of BML-111 on NF-κB pathway during acute lung injury induced by hemorrhagic shock and resuscitation in rats.Methods Thirty-two adult male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 4 groups (n =8 each) using a random number table:sham operation group (group S),hemorrhagic shock and resuscitation group (group HSR),BML-111 group,and BML-111 + BOC-2 (lipoxin A4 receptor antagonist) group (group BOC-2).The animals were anesthetized with intraperitoneal pentobarbital sodium.Hemorrhagic shock was induced by blood letting and maintained for 30 min.The animals were then resuscitated for 30 min by infusion of the shed blood and lactated Ringer's solution.In group BOC-2,BOC-2 (50 μg/kg) was injected intraperitoneally before blood letting.In BML-111 and BOC-2 groups,BML-111 (1 mg/kg) was injected intraperitoneally at the beginning of resuscitation.The rats were sacrificed at 2 h after the end of resuscitation and lungs were removed for determination of pathological changes,myeloperoxidase (MPO) activity,intercellular adhesion molecule-1 (ICAM-1) expression (by immunohistochemistry),tumor necrosis factor-alpha (TNF-α) content (by ELISA),and NF-κB p65 and IκB-α expression (by Western blot).Results Compared with group S,the MPO activity,ICAM-1 expression,and TNF-α content were significantly increased,NF-κB p65 expression was up-regulated,and IκB-α expression was down-regulated in group HSR.Compared with group.HSR,the MPO activity,ICAM-1 expression,and TNF-α content were significantly decreased,NF-κB p65 expression was down-regulated,IκB-α expression was up-regulated,and pathological changes of lung were attenuated in group BML-111.Compared with group BML-111,the MPO activity,ICAM-1 expression,and TNF-α content were significantly increased,NF-κB p65 expression was up-regulated,and lκ:B-α expression was down-regulated,and pathological changes of lung were aggravated in group BOC-2.Conclusion BML-1 11 inhibits activation of NF-κB pathway and inflammatory responses,thus mitigating acute lung injury induced by hemorrhagic shock and resuscitation in rats.
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Objective To evaluate the effects of dexmedetomidine on the permeability of blood-brain barrier in rats subjected to global cerebral ischemia-reperfusion (I/R).Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each):sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP was maintained at 35-45 mm Hg) in anesthetized rats.In group D,dexmedetomidine was infused at a rate of 3μg· kg-1 · h-1 until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was injected intravenously immediately after onset of I/R.The rats were sacrificed at 24 h of reperfusion and their brains were immediately removed for microscopic examination of hippocampal CA1 region and for determination of the cell apoptosis,brain water content,Evans blue content and aquaporin 4 (AQP4) expression.Results The number of apoptotic cells was significantly larger,and brain water content,Evans blue content and AQP4 expression were higher in groups I/R and D than in group S (P ＜ 0.05 or 0.01).The number of apoptotic cells was significantly smaller,and brain water content,and Evans blue content and AQP4 expression were lower in group D than in group I/R (P ＜ 0.05 or 0.01).Global cerebral I/R-induced pathological changes were significantly attenuated in group D.Conclusion Dexmedetomidine can decrease the permeability of blood-brain barrier and attenuate global cerebral I/R injury in rats,and down-regulation of AQP4 expression may be involved in the mechanism.
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Objective To evaluate the effects of aspirin-triggered lipoxin A4 (ATL) on lipopolysaccharide (LPS)-induced acute lung injury in mice.Methods Thirty male SPF BALB/C mice,aged 10-12 weeks,weighing 25-30 g,were randomly assigned into 3 groups (n =10 each):normal saline group (group NS),LPS group and ATL groups.ATL 0.1 ml was injected via the tail vein 1 h after intra-tracheal instillation of 3 mg/kg LPS in LPS group.In ATL group,ATL 0.2 mg/kg was injected via the tail vein 1 h after intra-tracheal instillation of 3 mg/kg LPS.At 24 h after instillation,the mice were sacrificed.Bronchoalveolar lavage fluid was collected for determination of the total cell count,proportion of the polymorphonuclear leukocytes,proportion of the mononuclear leukocytes,and concentrations of the total protein,TNF-αt,IL-6,monocyte chemoattractant protein-1 (MCP-1) and IL-10.Lungs were removed for determination of myeloperoxidase (MPO) activity,phosphorylation of p38 mitogenactivated protein kinase (p38 MAPK),c-Jun N-terminal kinase (JNK),and extracellular signal-regulated kinase 1/2 (ERK1/2) in lung tissues and for microscopic examination.The pathological changes of lungs were scored.Results Compared with NS group,the lung injury scores,total cell counts,proportion of polymorphonuclear leukocytes,and concentrations of TNF-α,IL-6 and MCP-1 were significantly increased,and the proportion of mononuclear leukocytes was decreased in LPS and ATL groups,and IL-10 concentrations were decreased,and the concentrations of the total protein,MPO activity,and phosphorylation of p38 MAPK,JNK and ERK1/2 were significantly increased in group LPS (P ＜ 0.05),and no significant change in the concentrations of the total protein,MPO activity,phosphorylation of p38 MAPK,JNK and ERK1/2 was found in group ATL (P ＞ 0.05).Compared with LPS group,the lung injury scores,total cell counts,proportion of polymorphonuclear leukocytes and the concentrations of the total protein,TNF-α,IL-6 and MCP-1 were significandy decreased,the proportion of mononuclear leukocytes and IL-10 concentration were increased,and MPO activity and phosphorylation of p38 MAPK and JNK were decreased (P ＜ 0.05),and no significant change in the phosphorylation of ERK1/2 was found in group ATL (P ＞ 0.05).Conclusion ATL can ameliorate LPS-induced acute lung injury by inhibiting activations of p38MAPK and JNK signal pathways in mice.
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Objective To evaluate the role of autophagy in the development of neuropathic pain (NP) in rats.Methods Thirty male Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 3 groups (n =10 each) using a random number table:sham operation group (sham group),NP group and rapamycin (autophagy inducer) group (Rap group).Intrathecal catheter was inserted into the subarachnoid space and advanced caudally until the tip reached L4,5 segment.NP was induced by ligation of the left L5 spinal nerve (SNL) in NP and Rap groups.The L5 spinal nerve was only exposed,but not ligated in group sham.At 30 min before ligation and 2 days after operation,rapamycin 60 μg was injected intrathecally via the intrathecal catheter in Rap group,while the equal volume of vehicle (5％ dimethyl sulfoxide) was injected in sham and NP groups.The mechanical and thermal pain thresholds were measured on 1,3,5 and 7 days after ligation (T-4).The rats were sacrificed after the last measurement of pain threshold at T4.The ipsilateral L5 segment of spinal dorsal horn was removed for examination of autophagosomes (using transmission electron microscope) and for determination of the expression of LC3 Ⅱ and p62 (by Western blot) and content of IL-1β (by ELISA).Results Compared with sham group,the mechanical pain threshold at each time point and thermal pain threshold at T2-4 were significantly decreased,and the LC3 Ⅱ and p62 expression and IL-1β content were increased at T4 in group NP (P ＜ 0.05).Compared with NP group,the mechanical pain threshold at each time point,thermal pain threshold at T2-4 and LC3 Ⅱ expression at T4 were significantly increased,and the p62 expression and IL-1β content were decreased at T4 in group Rap (P ＜ 0.05).Microscopic examination showed that autophagosomes were observed in the spinal dorsal horn in NP and Rap groups,and the damage to organelles was lighter in Rap group than in NP group.Conclusion The development of NP is related to autophagic dysfunction in rats.
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Objective To evaluate the effects of different types of acute respiratory distress syndrome (ARDS) on high frequency oscillatory ventilation (HFOV)-improved extravascular lung water and pulmonary vascular permeability in piglets.Methods Twelve healthy piglets,weighing 15-20 kg,were randomly allocated into 2 groups (n =6 each) using a random number table:endogenous ARDS (P group) and exogenous ARDS (EXP group).Anesthesia was induced with midazolam and propofol.The tracheal tube was inserted.Anesthesia was maintained with iv infusion of propofol and fentanyl.ARDS was induced with normal saline infused via the tracheal tube in group P.ARDS was induced with oleic acid 0.05 ml/kg injected intravenously over 45-60 min in group EXP.Then 4 h of HFOV was performed.Before ARDS (T0),immediately after ARDS (Ti) and at 1,2,3 and 4 h of HFOV (T2-5),arterial blood samples were collected for blood gas analysis and the variables such as extravascular lung water index (EVLWI),pulmonary vascular permeability index (PVPI),and extravascular lung water (EVLW)/intra thoracic blood volume (ITBV) were monitored.The oxygenation index (PaO2/FiO2) was calculated.Results Compared with the baseline value at T0,the oxygenation index was decreased at T1,and the oxygenation index was less than 200 mm Hg in the two groups (P ＜ 0.05).There was no significant difference in the maximum degree of changes in EVLWI,PVPI and EVLW/ITBV between the two groups (P ＞ 0.05).Conclusion Endogenous and exogenous ARDS disease factor does not affect HFOV-improved extravascular lung water and pulmonary vascular permeability in piglets.
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Objective To evaluate the effects of penehyclidine hydrochloride (PHC) on the expression of Toll like receptor-4 (TLR4) and nuclear factor kappa B (NF-κcB) in a rat model of sepsis-induced acute lung injury (ALI).Methods Seventy-two adult male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 3 groups (n =24 each) using a random number table:shame operation group (group S),ALI group and PHC group.Sepsis-induced ALl was induced by cecal ligation and puncture in anesthetized rats.In group PHC,PHC 0.45 mg/kg was intramuscularly injected immediately after cecal ligation and puncture.At 6,12,24 and 36 h after ligation,the broncho-alveolar lavage fluid (BALF) was collected for detection of TNF-α and IL-6 concentrations and the lungs were removed for determination of the expression of TLR4 (using RT-PCR and Western blot) and NF-κBp65 (using Western blot) in lung tissues and for microscopic examination.The pathological changes of lungs were scored.The wet to dry lung weight (W/D) ratio was calculated and the activity of myeloperoxidase (MPO) in lung tissues was measured.Results As compared with S group,the IL-6 concentrations in BALF at 6,12 and 24 h after ligation,TNF-α concentration in BALF at 6 and 12 h after ligation,and the expression of TLR4 and NF-κBp65,pathological scores,W/D ratio and MPO activity at each time point were significantly increased in ALI group (P ＜ 0.05).Compared with ALI group,the TNF-α concentration in BALF at 6 and 12 h after ligation,and IL-6 concentrations in BALF,the expression of TLR4 and NF-κBp65,pathological scores,W/D ratio and MPO activity at each time point were significantly decreased in group PHC (P ＜ 0.05).Conclusion PHC inhibits NF-κB activation and decreases inflammatory responses through blocking TLR4 expression in lung tissues,thus attenuating sepsis-induced ALI in rats.
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Objective To determine whether p38 mitogen-activated protein kinase (p38MAPK) signaling pathway is involved in cerebral fractalkine-induced hyperalgesia in mice.Methods Two hundred and twenty-five male Kunming mice weighing 30-40 g were randomly divided into 4 groups:group control ( group C,n =55 ) ;group fractalkine (group F,n =60); group anti-CX3CR1 + fractalkine (group CF,n =55) and group SB203580 (p38MAPK inhibitor) + fractalkine (group SF,n =55).Fractalkine 100 ng was injected into cerebral lateral ventricle (i.c.v.) in groups F,CF and SF.Anti-CX3CR1 1 μg and SB203580 1 μg were injected i.c.v.at 1 h before fractalkine injection in groups CF and SF respectively.Paw withdrawal latency to a thermal nociceptive stimulus (PWL) was measured at 30 min before the drugs were injected into cerebral lateral ventricle and 30,60,120 and 240 min after fractalkine injection.Five animals were sacrificed after PWL measurement at each time point and their brains were removed for determination of phosphorylated p38MAPK protein expression (by Western blot analysis).Five animals were sacrificed at 30 min before the drugs were injected into cerebral lateral ventricle and 6,12 and 24 h after fractalkine injection for determination of IL-1β and TNF-α contents in the brain (by ELISA) in all the 4 groups.In group F 5 animals were sacrificed at 4 h after fractalkine injection for determination of action of fractalkine on microglia or astrocyte (by immunofluorescence).Results Fractalkine i.c.v.injection significantly reduced PWL and increased phosphorylated 38MAPK,IL-1β and TNF-α levels in group F as compared with group C.Pretreatment with anti-CX3CR1 or SB203580 significantly decreased fractalkine-induced hyperalgesia and phosphorylated-p38MAPK,IL-1β and TNF-α levels in groups CF and SF as compared with group F.Fractalkine was localized at microglia.Conclusion p38MAPK signal transduction pathway is involved in cerebral fractalkine-induced hyperalgesia in mice.
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Objective To compare the hypnotic effect of propofol administered by target-controlled infusion (TCI) during day-time and night-time,in order to explore the effect of circadian rhythms on the sedative effect of propofol.Methods Sixty-five male ASA Ⅰ or Ⅱ patients aged 18-55 yr undergoing emergency minor hand surgery were divided into 2 gorups according to the time of the day when they received propofol TCI:day-time group (from 7:01 to 19:00) and night-time group (from 19:01 to 7:00).The pharmacokinetic parameters proposed by Schnider which predict effect-site concentration (Ce) were used.Four effect-site concentrations of propofol were set:0.8,1.2,2.0 and 4.0 μg/ml.Ce was increased step by step and each Ce was maintained for 5 min.The level of sedation at each Ce was assessed by BIS and OAA/S scores.BIS value and Ce of propofol were recorded and compared between the 2 groups when the patients lost consciousness (OAA/S score =2).Results There was 28 and 30 patients in day-time and nighet-time groups respectively.When Ce =1.2 and 2.0 μg/ml,the BIS values were significantly lower in night-time group than in day-time group.There was no significant difference in BIS value between the 2 groups when Ce =0.8 and 4.0 μg/ml.When the patients lost consciousness (OAA/S =2),the BIS value was comparable between the 2 groups,but Ce was significantly lower in night-time group than that in daytime group.Conclusion The hypnotic effect of propofol is greater during night-time than during day-time.
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Objective To investigate the effects of valproic acid (VPA) on acute lung injury induced by Lipopolysaccharide in rats. Method The rat model of acute lung injury was made by intravenous injection of lipopolysaccharide (LPS). The pathological changes of lung were observed under light microscope and inflammatory cytokines in serum detected by using ELISA to judge whether the model was successfully done or not. All rats were divided into three groups as per the different intervention agents employed. Rats in control group were treated with intravenous injection of NS in dose of 5 ml/kg, rats in LPS group were exposed to LPS with dosage of 10 mg/kg and model rats in LPS + VPA group were treated with VPA in dose of 300 mg/kg. The rats were sacrificed 6 h after LPS or NS administration. The blood PaO2 ,A-aDO2 and blood lactic acid (Lac) were measured, the lungs were removed for observing the histopathological changes and determination of wet/dry lung weight (W/D) ratio and myeloperoxidase (MPO) activity as well as albumin concentration in broncho-alveolar lavage fluid (BALF) . Seurm was collected to determine the concentrations of tumor necrosis factor-a (TNF-α) and interleukin-1β( IL-1 β) by using LISA 6 h later. All data were presented in ((x)±s). One-way ANOVA was used for comparing differences between groups. Results Compared with acute lung injury group, the blood PaO2 (94. 50 ± 4.38 ) in rats of LPS + VPA group was higher, whereas A-aDO2 ( 13.50 ± 4.77 ) and blood lac( 2.13 ± 1. 02 ) in LPS + VPA group were lower. VPA significantly lowered W/D (5.33 ±0. 12) ratio and MPO activity (4.38 ±0. 42) in the lung. Albumin concentration ( 1. 260 ± 0. 039 ) in BALF, and the levels of TN F-α( 2 410 ±320 )and IL-1β( 1 220 ± 162 )in serum were lower in LPS + VPA group. The histological changes of lung injury were lessened by VPA. Conclusions Valproic acid has protective effects against lipopolysaccharide-induced acute lung injury in rats.
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ObjectiveTo investigate the effect of ketamine on nicotine-induced current in rat superior cervical ganglion neurons.MethodsNewborn Wistar rats were used in this study.Neurons were isolated enzymatically from superior cervical ganglia of newborn rats in an aseptic condition and cultured in 90％ DMEM/F12,10％ horse serum containing penicillin 100 μg/ml for 5-7 d.Nicotine-induced current was measured and recorded using whole-cell patch clamp technique.A mixture of nicotine 50 μmol/L and different concentrations of ketamine ( 10,25,50,100 μmol/L) was added to the isolated neurons.The effect of ketamine on nicotine-induced current was evaluated.ResultsNicotine-induced peak current was inhibited by ketamine in a concentration-dependent manner.The time constant of fast and slow desensitizing phase of the nicotine acetylcholine receptor was shortened after being exposed to the mixture of nicotine 50 μmol/L + 50 or 100 μmol/L ketamine as compared to nicotine 50 μmol/L-induced current.The median effective concentration of ketamine inhibiting nicotine-induced current was less than 20 μmol/L.ConclusionKetamine can decrease nicotine-induced current in rat superior cervical ganglion neurons in a concentration-dependent manner indicating that inhibition of sympathetic activity is involved in the mechanism of decrease in BP by ketamine in specific condition.
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Objective To investigate the effects of dexmedetomidine on global cerebral ischemia-reperfusion (I/R) injury in rats.Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n =18 each): shame operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral I/R was produced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mm Hg).In group D dexmedetomidine 3 μg/kg was injected iv immediately after I/R,followed by infusion of dexmedetomidine at a rate of 3 μg· kg- 1 · h- 1 until 2 h of reperfusion.The neurological deficit score (NDS) was assessed (0 =normal,100 =brain death) at 6 h (T1),24 h (T2)and 72 h (T3) of reperfusion.Then six rats were sacrificed in each group and brain tissues were removed for microscopic examination of hippocampus CA1 region and determination of activity of myeloperoxidase (MPO),contents of TNF-α and IL-1β and expression of glial fibrillary acidic protein ( GFAP).Results Compared with group S,NDS,MPO activity and the contents of TNF-α and IL-1β at T1-3 were significantly increased,the expression of GFAP was up-regulated at T2,3 in groups I/R and D ( P ＜ 0.05 or 0.01).Compared with group I/R,NDS,MPO activity and TNF-α concent were significantly decreased at T1-3,IL-1β concent was decreased at T1,2,the expression of GFAP was down-regulated at T2,3 in group D (P ＜ 0.05 or 0.01 ).The pathologic changes were significantly attenuated in group D as compared with group I/R.Conclusion Dexmedetomidine can attenuate global cerebral I/R injury in rats,and the inhibition of inflammatory response may be involved in the mechanism.
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Objective To investigate the effect of lipoxin A4 ( LXA4 ) on the permeability of blood-brain barrier (BBB) after focal cerebral ischemia-repeffnsion (I/R) in rats. Methods Fifty-four adult male SD rats weighing 200-250 g were randomly divided into 3 groups ( n = 18 each): group Ⅰ sham operation (group S); group Ⅱ focal cerebral I/R ( group I/R) and group Ⅲ LXA4 ( group L). Focal cerebral I/R was produced by middle cerebral artery occlusion (MCAO) with a 4-0 nylon thread with rounded tip inserted into right internal jugular vein and threaded cranially in group Ⅱ and Ⅲ . In group Ⅲ LXA4 100 ng was injected into right lateral ventricle of the brain after MCA was successfully occluded. MCAO was maintained for 2 h. The neurological deficit was evaluated and scored (0 = no deficit, 5 = death) at 24 h of reperfusion. 2% Evans blue 4 ml/kg was injected via femoral vein at 1 h before the animals were sacrificed. The animals were killed and their brains were immediately removed for determination of brain water content, Evans blue content and expression of matrix metalloproteinase-9 (MMP-9)in the ischemic cortex. Results The neurologic deficit scores, the brain water and Evans blue content and MMP-9 protein expression in the cortex were significantly higher in I/R group than in S group. The cerebral I/R-induced changes were significantly attenuated in LXA4 group. Conclusion LXA4 can protect blood-brain barrier against cerebral I/R injury by inhibiting MMP-9 protein expression in the brain tissue.
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Objective To investigate the effect of lipoxin A4(LXA4) on inflammatory response in a rat model of permanent focal cerebral ischemia (PFCI). Methods Seventy-two adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n = 24 each):group Ⅰ sham operation (group S); group Ⅱ PFCI and group Ⅲ LXA4. PFCI was induced by thread occlusion of right middle cerebral artery according to the method described by Longa in group Ⅱ and Ⅲ. In group Ⅲ LXA4 100 ng/5 μl was injected into right ventricle of the brain after PFCI was successfully induced, while in group Ⅰ and Ⅱ equal volume of normal saline was injected instead of LXA4. Six animals were killed at 6, 12 and 24 h of ischemia. Their brains were immediately removed for microscopic examination and determination of myeloperoxidase (MPO) activity, TNF-α, IL-10 and transforming growth factor-β1 (TGF-β1) contents in the ischemic cortex. The expression of glial fibrillary acidic protein (GFAP)was measured by immuno-histochemistry. Apoptosis in neurons was assessed using TUNEL. Results PFCI significantly increased MPO activity, TNF-α, IL-10 and TGF-β1 contents and GFAP expression in the ischemic cortex and neuronal apoptosis in group Ⅱ as compared with group S. LXA4 significanfly decreased MPO activity,TNF-α content, GFAP expression and neuronal apoptosis and increased IL-10, TGF-β1 contents at 12,24 h of ischemia. LXA4 significantly ameliorated PFCI-induced cerebral histopathologic damage. Conclusion LXA4 can protect the brain against PFCI injury by inhibiting inflammatory response.
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Objective To investigate the effects of erythropoietin (EPO) pretreatment on the acute lung injury induced by lipopolysaccharide (LPS) in rats and the underlying mechanism. Methods Thirty-two male SD rats weighing 180-220 g were randomly divided into 4 groups (n=8 each): group Ⅰ control (C);group Ⅱ EPO;group Ⅲ LPS and group Ⅳ EPO + LPS. EPO 3 000 U/kg was given IP in group Ⅱ , LPS 6 mg/kg was given iv in group Ⅲ . In group Ⅳ EPO 3 000 U/kg was given IP at 30 rain before iv LPS 6 mg/kg, The animals were killed at 4 h after LPS administration. Lung tissue specimens were obtained for microscopic examination. Wet/dry ratio (W/D), myeloperoxidase (MPO) activity, malondialdehyde (MDA) and nitric oxide (NO) content in lung tissue were determined. The expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine (NT) in lung tissue was determined by Western blot. Results W/D ratio, MPO activity, MDA and NO content were significantly increased and iNOS and NT expression was significantly up-regulated in LPS group as compared with control group. EPO pretreatment significantly attenuated the LPS-induced changes in group EPO + LPS. Conclusion EPO pretreatment can ameliorate the acute lung injury induced by LPS by down-regulating iNOS expression and reducing NO production.