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Objective To investigate the effect of Neostigmine on Mivacurium Chloride in postoperative recovery of elderly patients with anesthesia.Methods A total of 46 patients (32 males,14 females,aged 60-73 years,ASA grade Ⅰ or Ⅱ) who underwent laparoscopic surgery for gastrointestinal tumor under general anesthesia,were randomly divided into two groups.Patients in the studying group (group A,n=22) were given a dosage of eostigmine 20 ug/kg after the end of surgery,and patients in control group (group B,n=24) were given 0.9% saline solution.Monitored the contract reaction of adductor pollicis through train-of-four ratio (TOFR) by stimulating ulnar nerve.Record condition of recovery from neuromuscular blocked,untoward effect after operation,the activity of the plasmacholinesterase at the time of induction of anaesthesia and extubation.Results The sex,age,height,weight,BMI,operation time,fluid volume,temperature,the activity of the plasmacholinesterase,recovery score and sedation score had no significant difference.Activity decline of the plasmacholinesterase is obviously related with infusion liquid volume,was statistically significant(P<0.05),group A is lower than group B obviously at the recovery of TOFR to 25%,to 70%,70% to 90%,onset time and recovery index time,was statistically significant (P<0.05),the difference of TOFR of the two groups was statistically significant at the time of 5 min、10 min、30 min after extubation (P<0.05).The difference of the incidence of TOFR<0.7 of the two groups at the time of 5 min,10 min,30 min after extubation and the difference of the incidence of TOFR<0.9 of the two groups at the time of 10 min,30 min after extubation were statistically significant (P<0.05).Conclusion There is obvious significance for neostigmine to resume muscle force in mivacurium chloride postoperative recovery in the elderly.
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Objective To evaluate the lung protection of remote limb ischemic preconditioning during one-lung ventilation (OLV) in the patients undergoing esophageal cancer resection.Methods Seventyone patients of both sexes,aged 30-64 yr,with body mass index of 15-28 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or Ⅱ,scheduled for elective esophageal cancer resection,were randomly divided into control group (group C,n =34) and remote limb ischemic preconditioning group (group RLIP,n =37) using a random number table.Patients in group RLIP received three cycles of 5-min ischemia/5-min reperfusion induced by a blood pressure cuff placed on one upper arm before OLV.Before OLV (T0),at 1 and 2 h of OLV (T1,2),at 20 min after re-expansion of the collapsed lung (T3),and at 2 h after operation (T4),blood samples were drawn from the radial artery for blood gas analysis,oxygenation index (PaO2/FiO2) and alveolar-arterial oxygen gradient (A-aDO2) were calculated.At T0,T2,T3 and T4,blood samples were collected from the radial artery for determination of plasma tumor necrosis factor-alpha (TNF-α),interleukin-6 (IL-6),and IL-10 concentrations.Results Compared with group C,PaO2/FiO2 was significantly increased,and A-aDO2was decreased at T1,2,the plasma TNF-α concentrations were decreased at T2-4 (P＜0.05),and no significant change was found in the plasma IL-6 and IL-10 concentrations and rate of abnormal pulmonary function at T1-4 in group RLIP (P＞O.05).Conclusion Although remote limb ischemic preconditioning can produce lung protection during OLV in the patients undergoing esophageal cancer resection,it provides no clinical significance.
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Objective To investigate the effect of remote ischemic postconditioning on brain injury after asphyxial cardiac arrest-resuscitation in rats.Methods Sixty-nine male Sprague-Dawley rats were randomly divided into 3 groups (n =23 each) using a random number table:sham operation group (group S),asphyxial cardiac arrest-resuscitation group (group CA-CPR),and remote ischemic postconditioning group (group RIPost).The animals were anesthetized with intraperitoneal 1％ pentobarbital 40 mg/kg,intubated and mechanically ventilated.Asphyxia was induced by occlusion of the tracheal tube and resuscitation was started 8 min later.In RIPost group,RIPost was produced by 3 cycles of 15 min occlusion of the right hind femoral artery-15 min release of the right hind femoral artery after restoration of spontaneous circulation (ROSC).Neurological deficits were evaluated and scored at 24 h,72 h and 7 days after ROSC.Neuron specific enolase (NSE) concentration in serum was assessed at 48 h after ROSC by ELISA.At 3 days after ROSC,the number of viable neurons in hippocampal CA1 region was recorded (by N issl's staining).Morris water maze test was used to quantify spatial learning and memory deficits after ROSC.Results Compared with group S,the neurological deficit score at each time point and the number of viable neurons in hippocampal CA1 region were significantly decreased,the NSE concentration in serum was increased,the escape lantency was prolonged,and the target quadrant residence time percentage and distance percentage were decreased in CA-CPR and RIPost groups.Compared with group CA-CPR,the neurological deficit score at each time point and the number of viable neurons in hippocampal CA1 region were significantly increased,the NSE concentration in serum was decreased,the escape lantency was shortoned,and the target quadrant residence time percentage and distance percentage were increased in group RIPost.The damage to neurons in hippocampal CA1 region was significantly mitigated in group RIPost as compared with group CA-CPR.Conclusion Remote ischemic postconditioning can reduce brain injury after asphyxial cardiac arrest-resuscitation in rats.
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Objective To evaluate the effect of isoflurane preconditioning on inflammatory responses during spinal cord injury (SCI ) in rats .Methods Sixty adult male Sprague-Dawley rats ,weighing 250-300 g , were randomly divided into 3 groups ( n= 20 each ) using a random number table :sham operation group (S group) , SCI group , and isoflurane preconditioning group (I group ) . The animals were anesthetized with intraperitoneal pentobarbital sodium 40 mg/kg .SCI was produced by a weight-drop contusion at the T10 level .The rats inhaled 2% isoflurane for 2 h ,and the model was established at 24 h after the end of isoflurane inhalation in I group . Neurological function was assessed and scored by using the the Basso , Beattie , Bresnahan (BBB ) Locomotor Rating Scale on 7 days after SCI .Five rats in each group were then chosen and spinal cord specimens were obtained and cut into sections which were stained with haematoxylin and eosin for determination of the viable neuron count .Fifteen rats in each group were sacrificed and the spinal cord was removed for detection of nuclear factor kappaB (NF-κB ) and interleukin-1β (IL-1β) expression (by Western blot ) .Results Compared with S group ,BBB score and the number of viable neurons were significantly decreased ,and the expression of NF-κB and IL-1βprotein was up-regulated in SCI group ( P<0.05) .Compared with SCI group ,BBB score and the number of viable neurons were significantly increased ,and the expression of NF-κB and IL-1βprotein was down-regulated in group I ( P<0.05 ) .Conclusion The mechanism by which isoflurane preconditioning protects the spinal cord is related to inhibition of inflammatory responses in rats .
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Objective To evaluate the efficacy of acting κ opioid receptor for prevention of high altitude pulmonary edema (HAPE) in rats.Methods Forty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 5 groups (n =8 each) using a random number table:control group (group C),hypobaric hypoxia group (group H),normal saline + hypobaric hypoxia group (group NH),U50488H (a selective kappa-opioid receptor agonist) + hypobaric hypoxia group (group UH),and nor-binaltorphimine (norBNI,a selective kappa-opioid receptor antagonist) + U50488H + hypobaric hypoxia group (group NUH).The rats were put into the hyperbaric chamber and exposed to hypobaric hypoxia (atmospheric pressure 355 mmHg,partial pressure of oxygen 74 mmHg) for 2 days to induce HAPE.At 3 days before HAPE,normal saline 0.5 ml,U50488H 1.25 mg/kg,and nor-BNI 2.0 mg/kg were injected intraperitoneally once a day in NH,UH,and NUH groups,respectively,and in addition U50488H 1.25 mg/kg was injected intraperitoneally 10 min later in NUH group.After 2 h exposure to hypobaric hypoxia,mean pulmonary artery pressure (mPAP) was detected,and arterial blood samples were collected for determination of serum malondialdehyde (MDA) and erythropoietin (EPO) levels.The rats were then sacrificed and lungs were removed for microscopic examination and for determination of the levels of nitric oxide (NO),inducible nitric oxide synthase (iNOS),MDA,superoxide dismutase (SOD),endothelin-1 (ET-1),thromboxane B2 (TXB2),and 6-keto-prostaglandin F1α (6-keto-PGF1α) in lung tissues.Lung water content and TXB2/6-keto-PGF1α ratio was calculated.Results Compared with group C,mPAP,lung water content,ET-1,MDA,TXB2 and 6-keto-PGF1α levels,TXB2/6-ketoPGF1α ratio,and serum MDA and EPO levels were significantly increased,and iNOS,NO and SOD levels were decreased in the other four groups (P ＜ 0.05).Compared with group H,mPAP,lung water content,ET-1,MDA,TXB2 and 6-keto-PGF1α levels,TXB2/6-ketoPGF1α ratio and serum MDA and EPO levels were significantly decreased,and iNOS,NO and SOD levels were increased in UH group (P ＜ 0.05),and no significant changes were found in the indexes mentioned above in NH and NUH groups (P ＞ 0.05).The pathological changes of lung tissues were significantly attenuated in group UH as compared with H group.Conclusion Acting κ opioid receptor can produce prevention for HAPE in rats,and inhibition of lipid peroxidation and correction of the imbalance between vasoconstrictive factors and vasodilative factors may be involved in the mechanism.
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Objective To investigate the effect of isoflurane preconditioning on Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88) signaling pathway in ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four healthy male SD rats,aged 3 months,weighing 250-280 g,were randomly divided into 3 groups (n =18 each):sham operation group (group S),I/R group and isoflurane preconditioning group (group IP).Focal cerebral I/R was induced by middle cerebral artery occlusion.In groups I/R and IP,a nylon thread with rounded tip was inserted into the right internal jugular vein and threaded cranially until resistance was met.The middle cerebral artery was occluded for 2 h,followed by 24 h reperfusion.In group IP,the animals inhaled 2.0％ isoflurane for 2 h,and middle cerebral artery occlusion was performed at 24 h after the end of preconditioning.Neurological deficit was scored at 24 h of reperfusion and then the rats were sacrificed.Five rats in each group were chosen and the brains removed for measurement of the cerebral infarct volume.The right cerebral ischemic penumbra was removed for detection of the expression of HSP60,TLR4,MyD88 protein and mRNA by Western blot analysis and real time-PCR.Apoptosis was detected in the ischemic penumbra in the left 3 rats in each group using TUNEL.Apoptosis index (AI) was calculated.Results Neurological deficit scores and AI were significantly increased,the cerebral infarct volume was significantly enlarged,and the expression of HSP60,TLR4,MyD88 protein and mRNA was up-regulated in groups I/R and IP as compared with group S ( P ＜ 0.05).Isoflurane preconditioning significantly reduced the cerebral infarct volume and decreased neurological deficit scores and AI,and down-regulated the expression of HSP60,TLR4,MyD88 protein and mRNA (P ＜ 0.05).Conclusion The mechanisn by which isoflurane preconditioning protects ischenic penumbra following focal cerebral I/R may be related to inhibition of TLR4-MyD88 signaling pathway.
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Objective To investigate the effect of intravenous infusion of hyper-oxygenated solution (HOS) on small intestinal ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty-four rabbits of both sexes,weighing 2.5-3.2 kg,were randomly divided into 3 groups ( n =8 each):sham operation group (group S),I/R group,and HOS group.Small intestinal I/R was produced by clamping the superior mesenteric artery (SMA) for 1 h followed by 2 h of reperfusion in I/R and HOS groups,while the SMA was only clamped in group S.HOS was infused intravenously at a rate of 20 ml· kg-1 ·h -1 via the auricular vein starting from the time immediately after clamping the SMA in group HOS and the equal volume of normal saline was infused instead of HOS in group I/R.Blood samples were obtained from the inferior vena cava at 2 h of reperfusion to detect the concentration of serum lactic acid.The animals were then sacrificed and the small intestine was removed for determination of the malondialdehyde (MDA) content,and activities of superoxide dismutase (SOD),catalase (CAT) and glutathione peroxidase (GSH-Px) in intestinal tissues and for microscopic examination.The pathological changes of the intestinal epithelia were observed and the damage.to the mucous membrane was scored.The internal organs were removed and bacterial translocation from gut to the internal organs was observed.Results Compared with group S,the level of MDA and lactic acid,and rate of bacterial translocation were significantly increased,and the activities of SOD,CAT and GSH-Px were significantly decreased in groups I/R and HOS ( P ＜ 0.05).Compared with group I/R,the level of MDA and lactic acid,rate of bacterial translocation,and activities of SOD,CAT and GSH-Px were significantly decreased in group HOS ( P ＜ 0.05).Conclusion Intravenous infusion of HOS can reduce small intestinal I/R injury in rabbits.
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Objective To investigate the effect of exogenous hydrogen sulfide on myocardial NF-κB signaling pathway in rats with hemorrhagic shock (HS).Methods Forty adult male rats,weighing 250-300 g,were randomly divided into 4 groups (n =10 each):sham operation group (Sham group),sham operation + NaHS group (Sham + NaHS group),HS group and HS + NaHS group.HS was induced by withdrawing blood from the femoral artery.After HS,NaHS 28 μmol/kg was injected intraperitoneally at 10 min before resuscitation in groups HS + NaHS and Sham + NaHS.MAP was monitored and recorded at 0,1.5,2,3,4 and 6 h after blood-letting.The rats were then sacrificed and hearts were removed for determination of phosphorylated IKKβ (pIKKβ),IκBα (pIκBα),NF-κB p65 (pNF-κB p65) and high-mobility group box 1 (HMGB1) and for examination of myocardial ultrastructure with light and electron microscope.Results Compared with Sham and Sham + NaSH groups,MAP was significantly decreased and the expression of pIKKβ,pIκBα,pNF-κB p65 and HMGB1 was up-regulated in HS and HS + NaHS groups (P ＜ 0.05).Compared with HS group,MAP was significantly increased and the expression of pIKKβ,pIκBα,pNF-κB p65 and HMGB1 was down-regulated in HS + NaHS group (P ＜ 0.05).The pathologic changes were attenuated in HS + NaHS group compared with group HS.Conclusion Exogenous hydrogen sulfide can attenuate myocardial injury induced by HS through inhibition of NF-κB signaling pathway and reduction of inflammatory response.
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Objective To evaluate the role of δ opioid receptor in the brain injury following asphyxial cardiac arrest-resuscitation in rats.Methods Ninety-six pathogen-free male Sprague-Dawley rats,weighing 300-350 g,were randomly divided into 4 groups (n =24 each):sham operation group (group S),asphyxial cardiac arrest-resuscitation group (group M),δ opioid receptor agonist BW373U86 group (group B) and δ opioid receptor antagonist naltrindole group (group N).Cardiac arrest was induced by clamping the tracheal tube for 8 min.Mechanical ventilation with pure oxygen was performed.Epinephrine 0.02 mg/kg and 5％ NaHCO3 1 mg/kg were injected intravenously as soon as chest compression was started.Appearance of spontaneous breathing and MAP ＞ 50 mm Hg (lasting for more than 10 min) were considered to be signs of successful recovery of spontaneous circulation (ROSC).BW373U86 and naltrindole 1 mg/kg were injected via the femoral vein immediately after ROSC in groups B and N,respectively,while the equal volume of normal saline was given instead in groups S and M.Neurological deficit score (NDS) was evaluated at 3,24 and 72 h after ROSC.The rats were then sacrificed,brains were isolated and the hippocampus was obtained for detection of the expression of brain-derived neurotrophic factor (BDNF)and tyrosine receptor kinase B (TrkB)mRNA by RT-PCR.The histological grading (HG) of neurons and number of survival neurons in hippocampal CA1 region were determined at 72 h after ROSC.Results Compared with group S,the expression of BDNF and TrkB mRNA was significantly up-regulated,HG was increased,and NDS and the number of survival neurons were decreased in groups M,B and N (P ＜ 0.05).Compared with group M,the expression of BDNF and TrkB mRNA was significantly up-regulated in group B,the expression of BDNF and TrkB mRNA was down-regulated in group N,and HG was significantly decreased,and NDS and the number of survival neurons were increased in groups B and N (P ＜ 0.05).NDS was significantly lower,the number of survival neurons was smaller,the expression of BDNF and TrkB mRNA was lower,and HG was higher in group N than in group B (P ＜ 0.05).Conclusion Activation of δ opioid receptor can reduce the brain injury following asphyxial cardiac arrest-resuscitation in rats and the mechanism may be related to up-regulation of BDNF and TrkB after activation of δ opioid receptor.
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Objective To investigate the effect of isoflurane preconditioning on the expression of 5-lipoxy-genase (5-LOX) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-nine male adult Sprague-Dawley rats weighing 250-300 g were randomly divided into 3 groups (n =13 each):sham operation group (group S); focal cerebral I/R group (group I/R); isoflurane preconditioning group (group Ⅰ).Focal cerebral I/R was produced by mid-cerebral artery occlusion in anesthetized rats.The rats inhaled 2 h of 2％ isoflurane and focal cerebral I/R was produced 24 h later in group I.The neurological deficits were scored at 24 h of reperfusion.The animals were then sacrificed.The brains were immediately removed for determination of the infarct size.The expression of 5-LOX,myeloid differentiation factor88 (MyD88) and nuclear factor kappa B (NF-κB) protein and mRNA was detected using Western blot and RT-PCR respectively.Results Compared with group S,the neurological deficit score was significantly increased,the infarct size was enlarged in groups I/R and I,the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was up-regulated in group I/R,and the expression of 5-LOX mRNA and MyD88 protein and mRNA was up-regulated in group I (P ＜ 0.05).Compared with group I/R,the neurological deficit score was significantly lower,the infarct size was smaller,and the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was lower in group I (P ＜ 0.05).Conclusion Isoflurane preconditioning can reduce focal cerebral I/R injury by down-regulating the expression of 5-LOX and inhibiting MyD88/NF-κB signaling pathway in rats.
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ObjectiveTo evaluate the biological characteristics of rat bone marrow mesenchymal stem cells (BMSCs) transfected with hypoxia-inducible factor-1α(HIF-1 α) gene.MethodsThe rat BMSCs of 3rd generation and the vector expressing HIF-1α gene (pcDNA3.1-HIF-1α) were provided by department of anesthesia,Tangdu Hospital,the 4th Military Medical University.BMSCs expressing HIF-1α gene (BMSCs-HIF-1α cells) were constructed by transfection of vector pcDNA3.1-HIF-1α into BMSCs by means of electroporation.Successful transfection of HIF-1α gene was confirmed by immuno-cytochemistry.Simple BMSCs and BMSCs-pcDNA3.1 cells were used as control cells.After being cultured in hypoxic condition HIF-1α expression was detected by Western blot analysis.Flow cytometry was used to determine the proportion of cells in G1,G2 and S phase and detect apoptosis.The proliferation index (PI) was calculated.The cell growth curve was described by MTT assay and the number of the 3 types of cells was recorded.ResultsA large number of deep blue granules were observed in the nuclei of BMSCs-HIF-1α cells using immuno-cytochemistry but no such granule was found in the two types of control cells.HIF-1α expression was significantly up-regulated and apoptosis rate (the number of apoptotic cella/the total number of cells examined) decreased in BMSC-HIF-1α cells compared with the control cells.The proportion of cells in S and G2 phase was significantly higher and the proportion of cells in G1 phase was significantly lower and PI higher in BMSCs-HIF-1α cells than in the control cells.The number of BMSCs-HIF-lα cells was significantly higher than the number of the two types of control cells at day 3-8 of culture.There was no significant difference in the above variables between BMSCs and BMSCs-pcDNA3.1 cells.ConclusionBMSCs-HIF-1α is successfully constructed by transfection of vector pcDNA3.1-HIF-1α gene into BMSCs by means of electroporation.
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Objectiye To investgate the effects of isoflurane preconditioning on expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) during focal cerebral ischemia-reperfusion (IR) in rats. Methods Thirty male SD rats weighing 250-300 g were randomly divided into 3 groups ( n = 10 each):sham operation group (group S);focal cerebral IR group and isoflurane preconditioning group (group IP). The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. In group IR and IP a nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. Mid-cerebral artery was occluded (MCAO) for 2 h followed by 24 h reperfusion. In group IP the animals inhaled 2% isoflurane98 % O2 for 1 h once a day for 5 consecutive days at 24 h before MCAO. Neurologic function was assessed and scored and cerebral infarct volume was measured at 24 h of reperfusion. The animals were sacrificed at 24, 48 and 72 h of reperfusion respectively. The right ischemic frontal lobes were removed for determination of TLR4, MyD88and NF-κB expression by Western blot analysis. Results MCAO significantly worsened neurologic function. The neurologic function deficit scores were significantly increased and the TLR4, MyD88 and NF-κB expression were significantly up-regulated in group IR as compared with group S (P ＜ 0.05). Isoflurane preconditioning significantly decreased cerebral infarct volumes and neurologic function deficit scores and down-regulated the expression of TLR4, MyD88 and NF-κB in group IP as compared with group IR ( P ＜ 0.05). Conclusion Isoflurane preconditioning can reduce inflammatory response and focal cerebral IR injury by down-regulating the expression of TLR4and Myd88.
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0.05),the escape latency was longer(P