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Objective:To evaluate the efficacy of remimazolam for induction and maintenance of general anesthesia in patients undergoing abdominal surgery.Methods:A total of 100 patients of both sexes, aged 18-64 yr, with body mass index of 18-30 kg/m 2, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ, undergoing elective abdominal surgery with general anesthesia requiring tracheal intubation, were enrolled in this study and divided into 2 groups ( n=50 each) using a random number table method: remimazolam group (group R) and propofol group (group P). Anesthesia was induced by intravenously infusing propofol 1.0-2.5 mg/kg in group P and remimazolam 0.15-0.35 mg/kg in group R. Sufentanil 0.4-0.5 μg/kg and rocuronium 0.6 mg/kg were intravenously injected in group R and group P. Anesthesia was maintained by intravenously injecting remimazolam 0.3-1.0 mg·kg -1·h -1 in group R and propofol 4-12 mg·kg -1·h -1 in group P. Remifentanil 8-15 μg·kg -1·h -1 was intravenously injected in group R and group P. Narcrotrend index (NI) was maintained at 37-64 (D 0-D 2). The success of sedation, time for loss of consciousness, time of disappearance of eyelash reflex, time when NI dropped to D 0, incidence of tidal volume, respiratory rate and apnea after the patients lost consciousness, duration of stay in post-anesthesia care unit, the fluctuation range of mean arterial pressure at 1, 3 and 5 min of induction, and the development of intraoperative and postoperative adverse events. Results:The success rate of sedation in group R and group P was 100%.Compared with group P, time for loss of consciousness, time of disappearance of eyelash reflex and time when NI dropped to D 0 were significantly prolonged, tidal volume and respiratory rate were increased, the incidence of apnea after the patients lost consciousness was decreased, awakening time was shortened, the incidence of intraoperative sinus bradycardia, injection pain and dream was decreased, fluctuation range of blood pressure at 1, 3 and 5 min of induction was decreased in group R ( P<0.05). Conclusion:Remimazolam can be safely and effectively used for induction and maintenance of general anesthesia in patients undergoing abdominal surgery, and its induction dose is 0.15-0.35 mg/kg, and maintenance dose is 0.3-1.0 mg·kg -1·h -1.
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Objective To evaluate the effect of sevoflurane preconditioning on the expression of metabotropic glutamate receptor type Ⅱ( mGluRⅡ) during focal cerebral ischemia-reperfusion ( I∕R) in rats. Methods Forty-eight clean-grade healthy male Sprague-Dawley rats were divided into 3 groups (n＝16 each) using a random number table method: sham operation group ( group S), cerebral I∕R group (group I∕R) and sevoflurane preconditioning group (group Sev). Rats were anesthetized with 10% chloral hydrate 3 ml∕kg. Focal cerebral I∕R was produced by occlusion of the right middle cerebral artery for 2 h fol-lowed by 24 h reperfusion. In group Sev, 2. 7% sevoflurane was inhaled for 1 h and 24 h later focal cerebral I∕R was produced. At 24 h after reperfusion, neurological deficit was scored, the cerebral infarct size was determined by TTC staining, the cell apoptosis in ischemic penumbra was observed by TUNEL, IκB-α ex-pression was detected by Western blot, and mGluRⅡexpression was determined by immunofluorescent stai-ning. The apoptosis rate was calculated. Results Compared with group S, the neurological deficit score, cerebral infarct size and apoptosis rate were significantly increased, the expression of mGluRⅡwas up-regu-lated, and the expression of IκB-α was down-regulated in I∕R and Sev groups ( P＜0. 05). Compared with group I∕R, the neurological deficit score, cerebral infarct size and apoptosis rate were significantly de-creased, the expression of mGluRⅡwas down-regulated, and the expression of IκB-α was up-regulated in group Sev (P＜0. 05). Conclusion Sevoflurane preconditioning reduces focal cerebral I∕R injury through inhibiting the expression of mGluRⅡ in rats.
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Objective:This study was aimed to compare the advantages and specifity of two different models to construct the animal model of preeclampsia in prague-Dawley(SD) rats.Methods:Female pregnancy SD rats were randomly divided into three groups (n =30 per group):Control group,STBM group and L-NAME + STBM group.The model of preeclampsia(PE) was established via intravenous or subcutaneous injection of STBM or L-NAME + STBM.In the STBM group,STBM were injected via the vena caudalis.In the L-NAME + STBM group,Nw-nitro-L-arginine-methyl ester(L-NAME) was injected subcutaneously.Control group got no treatment.Proteinuria(U-TP),blood pressure(BP),coagulation parameters (APTT,PT,and D-D) were tested at different times.Placental sections were histopathologically examined by H-E stanning.SFIt-1,SEng,PLGF mRNA and protein expression in placenta were tested by Real time PCR and Western blot respectively.Placental trophoblast cells were isolated and cultured,for advanced functional experiment.Results:There was no significant difference in U-TP,BP,APTT,PT and D-D between the 3 groups on pregnant 10D(P＞0.05),when compared with STBM group,U-TP,APTT,PT and D-D were significantly increased in STBM + L-NAME group on pregnant 15 d and 20 d (P ＜0.05),and there was no significant change in control group.The expression of SFlt-1,SEng mRNA and protein were significantly different between the 3 groups (P ＜ 0.05).The expression of sFIt-1,SEng mRNA and protein were significantly higher in STBM + L-NAME groupthan that in STBM group(P ＜ 0.05),with sigficantly reduced PLGF mRNA and protein in STBM + L-NAME group(P ＜0.05).There was a significant difference between the 3 groups in functional experiment(P＜0.05).The cell proliferation and invasion rate was lowest and the apoptosis rate was highest,with significant difference when compared to those in STBM group(P ＜ 0.05).Conclusions:STBM combined with L-NAME was more specific than STBM alone,to construct the model of preeclampsia in SD rats and provide a reliable basis for clinical diagnosis and treatment of preeclampsia.
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Objective:This study was aimed to compare the advantages and specifity of two different models to construct the animal model of preeclampsia in prague-Dawley(SD) rats.Methods:Female pregnancy SD rats were randomly divided into three groups (n =30 per group):Control group,STBM group and L-NAME + STBM group.The model of preeclampsia(PE) was established via intravenous or subcutaneous injection of STBM or L-NAME + STBM.In the STBM group,STBM were injected via the vena caudalis.In the L-NAME + STBM group,Nw-nitro-L-arginine-methyl ester(L-NAME) was injected subcutaneously.Control group got no treatment.Proteinuria(U-TP),blood pressure(BP),coagulation parameters (APTT,PT,and D-D) were tested at different times.Placental sections were histopathologically examined by H-E stanning.SFIt-1,SEng,PLGF mRNA and protein expression in placenta were tested by Real time PCR and Western blot respectively.Placental trophoblast cells were isolated and cultured,for advanced functional experiment.Results:There was no significant difference in U-TP,BP,APTT,PT and D-D between the 3 groups on pregnant 10D(P＞0.05),when compared with STBM group,U-TP,APTT,PT and D-D were significantly increased in STBM + L-NAME group on pregnant 15 d and 20 d (P ＜0.05),and there was no significant change in control group.The expression of SFlt-1,SEng mRNA and protein were significantly different between the 3 groups (P ＜ 0.05).The expression of sFIt-1,SEng mRNA and protein were significantly higher in STBM + L-NAME groupthan that in STBM group(P ＜ 0.05),with sigficantly reduced PLGF mRNA and protein in STBM + L-NAME group(P ＜0.05).There was a significant difference between the 3 groups in functional experiment(P＜0.05).The cell proliferation and invasion rate was lowest and the apoptosis rate was highest,with significant difference when compared to those in STBM group(P ＜ 0.05).Conclusions:STBM combined with L-NAME was more specific than STBM alone,to construct the model of preeclampsia in SD rats and provide a reliable basis for clinical diagnosis and treatment of preeclampsia.
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Objective To evaluate the effects of isoflurane anesthesia on the cognitive function and expression of translocator protein 18 kDa ( TSPO) in the brain tissues of aged rats. Methods Twelve pathogen?free male Sprage?Dawley rats, aged 20 months, weighing 500-550 g, were randomly divided into 2 groups ( n=6 each) using a random number table: control group ( group C) and isoflurane anesthesia group ( group I) . The rats inhaled 2% isoflurane in 100% O2 for 4 h in group I, or 100% O2 for 4 h in group C. The rats underwent Morris water maze test at 24 h after anethesia. The escape latency and frequency of crossing the original platform were recorded. Then the rats were sacrificed, and the hippocampus and cerebral cortex were isolated for determination of the expression of TSPO and Iba1 by Western blot and quantitative real?time reverse transcriptase?polymerase chain reaction. Results Compared with group C, the escape latency was significantly prolonged, the frequency of crossing the original platform was decreased, and the expression of TSPO and Iba1 protein and mRNA in the hippocampus and cerebral cortex was up?regulated in group I ( P<0. 05 ) . Conclusion Isoflurane anesthesia results in decreased cognitive function through up?regulating the expression of TSPO in the brain tissues of aged rats.
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Objective To investigate the effect of placenta derived tumor necrosis factor (TNF)-α and myostatin (MSIN) in patients with preeclampsia (PE) and fetal development.Methods One hundred and twenty pregnant women who delivery from October 2008 to October 2013 were enrolled in this study.In them,40 healthy pregnant women was normal control group,40 PE and fetal growth in normal pregnant women was PE group,40 PE and fetal growth restriction (FGR) of pregnant women was PE + FGR group.The immunohistochemical localization of SABC method was used to detect for TNF-α and MSIN protein in placenta tissue in each group respectively.Real-time fluorescent quantitative PCR and Western blotting were used to detect for TNF-α and MSIN mRNA and protein in placenta tissue.Results The TNF-α mainly located in placental blood vessels surrounding stroma,decidual cells,trophoblastic cells and MSIN mainly located in placental blood vessels surrounding stroma,decidual cells and terminal villi.The TNF-α and MSIN mRNA expression quantity in PE group was 3.65 ±0.86,1.80 ±0.32 ; in PE + FGR group was 3.88 ± 0.71,2.01 ± 0.55 ; in normal control group was 1.32 ± 0.21,0.77 ± 0.39.The TNF-α and MSIN mRNA expression quantity in PE group and PE + FGR group were significantly higher than those in normal control group(P ＜ 0.01),and there were significant differences between PE group and PE + FGR group(P ＜ 0.05).The TNF-α and MSIN protein expression in normal control group was 0.56 ±0.13,1.31 ± 0.23;in PE group was 1.67 ±0.25,1.55 ±0.34 ;in PE + FGR group was 2.78 ±0.41,3.07 ±0.51.The TNF-α and MSIN protein expression in PE group and PE + FGR group were significantly higher than those in normal control group(P ＜ 0.01),and there were significant differences between PE group and PE + FGR group(P ＜ 0.05).Conclusions The placenta derived TNF-α and MSIN have more important roles in the pathogenesis of PE and normal development of fetal.It can provide coping strategies by detecting the level of placenta derived TNF-α and MSIN.
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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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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 relationship between the expression of MIF mRNA and TNF-α in the lung tissue of rats with acute necrotizing pancreatitis (ANP) and explore their mechanism of action in acute lung injury during the course of ANP. Methods A total of 40 Sprague-Dawley rats were randomly divided into four groups (n = 10 in each group) : the sham operation (SO) group, ANP 3h group, 6h group, 12h group. The model of ANP was induced by retrograde injection of 5% sodium tanrocholate (0. 1 ml/100 g) into the biliary and pancreatic duct. The level of serum amylase was determined;pancreatic and lung tissues were harvested for pathological examination, and wet/dry weight ratios were estimated. Intrapulmonary expression of MIF mRNA was assayed by semi-quantitative RT-PCR. TNF-α in pulmonary homogenate was measured by immunoradiometric assay. Results Serum amylase, wet/dry weight ratios of pancreatic and lung tissues all significantly increased, and pathological injuries aggravated with time in ANP groups. Levels of TNF-α in ANP 3h, 6h, 12h group were (0.69 ± 0. 107) ng/ml, (1.64 ± 0. 10) ng/ml and (0.92 ± 0.11) ng/ml, and expression of MIF mRNA were 1.97±0.09, 2.55±0.23, 3.29±0.26, which were significantly higher than those in control group [(0. 19±0.06)ng/ml, 1.21±0.34, P<0.01]. lntrapulmonary expression of MIF mRNA was positively associated with lung pathological injuries, wet/dry weight ratio, and TNF-α(r = 0. 637, r = 0.684, r = 0.858, P < 0.01). Intrapulmonary levels of TNF-α was positively associated with lung pathological injuries, wet/dry weight ratio (r=0.540, r=0.421, P<0.01). Conclusions MIF mRNA was over- expressed and level of TNF-α was significantly increased in pulmonary tissue in rats with ANP, and this may be one of the mechanisms in the pathogenesis of lung injury in ANP.
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[Objective]To study the effect of arthroscopic reconstruction of anterior cruciate ligament with hamstring tendons and mini-plates.[Method]Thirteen cases of anterior cruciate ligament ruptures were reconstructed arthroscopically with over six strands of hamstring tendons in way of one-bundle and two-tunnel reconstruction.The grafts were fixed with suspension technique by mini-plates.The patients were followed up for one year.The clinical results were evaluated according to Lysholm rating scale.[Result]Twelve patients(92.31%) had negative Lachman test,and one patient showed positive Lachman test.Pivot shift test was negative in 12 cases,and was positive in one case.The Lysholm score increases from 47.77?1.96 to 95.38?4.74(P
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BACKGROUND: Degenerated cervical intervertebral discs can release many kinds of cytokines and inflammatory mediums, which plays an important role in onset and development of cervical syndrome.OBJECTIVE: To observe the effect of anti-cytokine Chinese herb combined with western drug (anti-hyperosteogeny capsule combined with glucosamine hydrochloride capsule) and gene therapy, on the contents of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) of degenerated cervical intervertebral discs in rabbits.DESIGN: Randomized controlled observation.SETTING: Department of Orthopaedics and Central Laboratory of Hebei People's Hospital.MATERIALS: The experiment was carried out in the Central Laboratory of Hebei People's Hospital from March 2003 to January 2004. A total of 35 New Zealand rabbits of both genders were selected and divided into 7groups according to randomly digital table: normal control group, shallowlayer model group, whole-layer model group, shallow-layer medicine group,whole-layer medicine group, shallow-layer gene group and whole-layer gene group. There were 5 rabbits in each group.METHODS: Except normal control group, rabbits in other 6 groups were used to establish models of dynamic dysequilibrium of cervical vertebra through cutting muscles of cervical back to induce degeneration of cervical intervertebral discs. Superficial group of muscle in cervical region was resected in shallow-layer groups, and both superficial and deep group of muscle was resected in whole-layer groups. ① Seven months after operation, rabbits in medicine groups were respectively treated with 1.1 g/kg anti-hyperosteogeny capsule (consisting of gouji, gusuibu, jixueteng, laifuzi,niuxi, nvzhenzi, roucongrong, shudihuang and yinyanghuo, etc.; Jiangsu Kangyuan Pharmaceutical Company Limited) and 0.06 g/kg glucosamine (Shanxi Zhongyuanwei Pharmaceutical Company Limited), which was dissolved into 20 mL distilled water. The medicine was administrated twice a day for 1 month. ② After anesthetization of rabbits in gene groups, recombinant plasmid DNA combined with transforming growth factor-β1 (TGF-β1) was injected to C2-3, C3-4 and C4-5 intervertebral disc (20μL per intervetebral disk). Eight months after modeling, rabbits in each group were sacrificed and C3-4 and C4-5 intervertebral disc was used as samples. In addition, contents of IL-1β and TNF-α were measured with double-antibodies-sandwich-ELISA method.MAIN OUTCOME MEASURES: Contents of IL-1β and TNF-α in cervical intervertebral discs of rabbits at 8 months after modeling.RESULTS: All 35 rabbits were involved in the final analysis. Eight months after modeling, for contents of IL-1β and TNF-α, shallow-layer model group was higher than normal control group (P ＜ 0.05-0.01); shallow-layer medicine group and shallow-layer gene group were obviously low er than shallow-layer model group (P ＜ 0.05); whole-layer medicine group and whole-layer gene group were lower than whole-layer model group (P＜ 0.05-0.01).CONCLUSION: The degenerated intervertebral discs can release many kinds of cytokine and inflammatory mediators which can enhance the degeneration of cervical intervertebral discs. Antihyperosteogeny capsule combined with glucosamine hydrochloride capsule and gene therapy can obviously reduce the contents of IL-1β and TNF-o in degenerated cervical intervertebral discs.