ABSTRACT
Objective@#: Dermoid cysts are uncommon in spinal cord tumors, and the phenomenon of their spontaneous rupture into the syrinx cavity is quite rare. We aimed to analyze the imaging characteristics and etiologies, and propose some surgical strategies, for this uncommon phenomenon. @*Methods@#: We retrospectively reviewed 14 cases with spinal dermoid cysts that ruptured into the cervical and thoracic syrinx cavity. There were six male and eight female cases, aged 21 to 46 years, who had lipid droplets in the syrinx cavity from C1 to L3. The dermoid cysts were always located at the conus. Based on patients’ complaints, clinical manifestations, and imaging results, we adopted tumor excision and/or syrinx cavity aspiration in one stage or multiple stages. @*Results@#: Three patients had only a syrinx cavity aspiration surgery due to a history of dermoid cyst excision. Eight patients had dermoid cyst resection and syrinx cavity aspiration in one stage. One patient was operated upon in two stages due to the development of new symptoms at nine months follow-up. Two patients underwent only tumor resection since they did not show similar symptoms or signs caused by the cervicothoracic syrinx. The axial magnetic resonance imaging indicated that the lipid droplets were always not at the center but were eccentric. The clinical effect was satisfactory during the follow-up period in this group. @*Conclusion@#: The lipid droplets filled the spinal syrinx cavity, not entirely confined to the central canal. Based on the chief complaints and associated signs, we adopted different surgical strategies and had satisfactory clinical results.
ABSTRACT
Objective:To analyze the effects of silver ion on the integration frequency of the class 1 integron in Escherichia coli ( E. coli) BL21(DE3) host. Methods:Two recombinant plasmids, pUCINT and pACINAD, were successively transformed into E. coli BL21 (DE3) to construct HS2 strains. Three experimental groups were set up using 0.3 μg/ml, 0.6 μg/ml and 0.8 μg/ml silver ion LB liquid medium, while control group used common LB liquid medium. Silver ion was supplied by silver nitrate and HS2 strains were cultured at 37℃ for 24 h. The copy number of cointegrates and the total copy number of integrons in each group were detected by real-time polymerase chain reaction (qPCR), and the ratio of them was the integration frequency. Changes in the integration frequency were analyzed by three independent phenotypic screening method and the protein expression in HS2 strains was analyzed by mass spectrometry. Results:The integration frequency in HS2 strains in the control group and three experimental groups (0.3 μg/ml, 0.6 μg/ml and 0.8 μg/ml silver ion) was 1.79×10 -5 (1.44×10 -5, 3.13×10 -5), 2.07×10 -5 (1.49×10 -5, 2.67×10 -5), 2.25×10 -6 (1.47×10 -6, 4.54×10 -6) and 1.69×10 -6 (0.22×10 -6, 3.08×10 -6), respectively. The integration frequency in the 0.6 μg/ml and 0.8 μg/ml silver ion groups was significantly lower than that in the control group ( P<0.01), but there was no significant difference between the 0.3 μg/ml silver ion group and the control group. Results of three independent phenotypic screening method were consistent with those obtained by qPCR. Mass spectrometry analysis showed that there were differences in protein expression in HS2 strains between the control group and the experimental groups. Conclusions:Silver ion at a certain concentration had an inhibitory effect on the frequency of drug resistance gene cassette captured by bacterial integron.
ABSTRACT
Objective To evaluate the efficacy of ultrasound-guided adductor canal block (ACB) for analgesia after tibial fracture.Methods American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes,aged 18-64 yr,with body mass index of 18-24 kg/m2,scheduled for elective internal fixation for unilateral tibial fracture under general anesthesia,were enrolled in this study.The tracheal tube was removed after operation,and then the patients were admitted to the postanesthesia care unit.The visual analog scale score was recorded.Eighty patients with visual analog scale score>3 were divided into 2 groups (n =40 each) using a random number table method:control group (group C) and ACB group.Patient-controlled intravenous analgesia (PCIA) was performed at the end of operation.Patients underwent ACB on the affected side,and 0.375% ropivacaine 20 ml was injected in group ACB.Sufentanil 0.1-0.2 μg/kg was intravenously injected in group C.Ramsay sedation scores were recorded immediately after entering the postanesthesia care unit (T0) and at 15 and 30 min and 1,2,4,8 12 and 24 h after block (T1-8).When visual analog scale scores >3 points and the pain could not be relieved through pressing the PCA pump,tramadol 1-2 mg/kg was intramuscularly injected.Patients were followed up for 24 h after surgery,and the postoperative consumption of sufentanil,pressing time of PCA and patients' satisfaction scores were recorded.The occurrence of postoperative nausea and vomiting,respiratory depression and hypoxemia and length of postoperative hospital stay were also recorded.Results Compared with group C,the postoperative consumption of sufentanil,pressing time of PCA,requirement for and consumption of tramadol,incidence of postoperative nausea and vomiting and oversedation,and Ramsay sedation score at T1-5 were significantly decreased,and the patients' satisfaction score were increased in group ACB (P<0.05).Conclusion Ultrasound-guided ACB exerts better analgesic efficacy after tibial fracture with fewer adverse reactions.
ABSTRACT
Objective To study the radiation injury of rat C6 glioma cell line by high resolution,1 H-nuclear magnetic resonance (1 H NMR) spectroscopy,and to preliminarily investigate its mechanism.Methods Metabolite concentrations in C6 cells were determined by 1 H NMR spectroscopy.Comet assay was used to evaluate DNA damage.Flow cytometry was used to determine the cell cycle and apoptosis rate.Colony-forming assay was used to measure the colony-forming rate and preliminarily investigate the mechanism of radiation injury.The resuhs were analyzed by one-way analysis of variance and Pearson correlation analysis.Results With the increase in radiation dose from 0 Gy to 1,5,10,and 15 Gy,DNA damage was enhanced in a dose-dependent manner (P=0.000-0.690);the percentage of cells in G1 phase increased (P =0.026-0.749);the apoptosis rate significantly increased (all P =0.000);the colony-forming rate significantly declined (P =0.000-0.004);the Lac/Cr ratio significantly decreased (P =0.000-0.015),which had a negative linear correlation with DNA damage parameters (tail length,r=-0.971;%DNA in the tail,r =-0.998;tail moment,r =-0.995) and apoptosis rate (r =0.978).Conclusions 1 H NMR spectroscopy reveals that the change in the Lac/Cr ratio is associated with injury and apoptosis of C6 cells after radiation.1 H NMR spectroscopy has the potential to predict radiation injury of glioma.
ABSTRACT
Objective To evaluate the role of extracellular signal-regulated kinase (ERK) signaling pathway in morphine-or sufentanil-induced inhibition of arrhythmia induced by myocardial ischemia-reperfusion (I/R) in rats and the relationship with connexin43 (Cx43).Methods Forty-eight healthy SPF adult male Sprague-Dawley rats,weighing 200-300 g,were randomly divided into 6 groups (n=8 each) using a random number table:sham operation group (group S);I/R group;morphine group (group M);sufentanil group (group Suf);morphine + ERK inhibitor PD98059 group (group MP);sufentanil + PD98059 group (group SP).Myocardial ischemia was induced by 30 min occlusion of the left anterior descending branch of the coronary artery,followed by reperfusion.In M and Suf groups,the animals were subjected to three cycles of 5-minute drug infusion (morphine 0.3 mg/kg and sufentanil 3 μg/kg,respectively) via the femoral vein interspersed with 5-minute drug-free periods starting from the time point immediately before ischemia.PD98059 10 mg/kg was injected intravenously at 10 min before ischemia in MP and SP groups.The development of ventricular arrhythmia was recorded within 30 min of ischemia and 30 min of reperfusion,and the arrhythmia was scored (AS).The animals were then sacrificed at 120 min of reperfusion,and the myocardial specimens were obtained for determination of the expression of total Cx43 (t-Cx43),phosphorylated Cx43 (p-Cx43),and phosphorylated ERK (p-ERK) by Western blot.Results Compared with group S,the AS was significantly increased,and the expression of p-Cx43 was significantly down-regulated in the other groups,and the expression of t-Cx43 and p-ERK was significantly down-regulated in I/R,SP and MP groups (P<0.05).Compared with group I/R,the AS was significantly decreased,and the expression of t-Cx43,p-Cx43 and p-ERK was significantly up-regulated in M and Suf groups (P < 0.05).Compared with M and Suf groups,the AS was significantly increased,and the expression of t-Cx43 and p-Cx43 was significantly down-regulated in SP and MP groups (P < 0.05).Conclusion The mechanism by which morphine or sufentanil inhibits arrhythmia induced by myocardial I/R is associated with up-regulated expression of myocardial Cx43 after activation of ERK signaling pathway in rats.
ABSTRACT
Objective To evaluate the role of mitochondrial permeability transition pore (mPTP) in hepatocytes in reduction of hepatic ischemia-reperfusion (I/R) injury by limb ischemic postconditioning in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 240-280 g,were randomly divided into 4 groups (n =12 each) using a random number table:sham operation group (group S);I/R group;limb ischemic postconditioning group (group LIPC);limb ischemic postconditioning and atractyloside group (group LIPC + APC).In I/R,LIPC and LIPC + APC groups,I/R injury was induced by 30 min occlusion of the hepatic artery and portal vein entering the left and middle lobes of the liver,followed by 120 min of reperfusion.The animals underwent 10 min of bilateral limb ischemia starting from 20 min after liver ischemia in group LIPC.In group LIPC+APC,the animals underwent 10 min of bilateral limb ischemia starting from 20 min after liver ischemia,and atractyloside 5 mg/kg was infused simultaneously via the penile vein.Blood samples were collected from inferior vena cava at the end of reperfusion to detect plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities.The rats were sacrificed,and the left lobe of the liver was removed to detect the degree of mPTP opening and to examine the ultrastructure of hepatocytes under electron microscope.Results Compared with group S,the plasma ALT and AST activities and degree of mPTP opening were significantly increased,and the damage to the ultrastructure of hepatocytes was obvious in the other three groups.Compared with group I/R,the plasma ALT and AST activities and degree of mPTP opening were significantly decreased,and the damage to the ultrastructure of hepatocytes was reduced in LIPC and LIPC + APC groups.Compared with group LIPC,the plasma ALT and AST activities and degree of mPTP opening were significantly increased in group LIPC+APC.Conclusion Limb ischemic postconditioning reduces hepatic I/R injury through inhibiting mPTP opening in hepatocytes of rats.
ABSTRACT
Objective To investigate the effects of propofol combined with remifentanil on he-patic ischemia-reperfusion injury in cirrhotic rats.Methods Sixty male SD rats of 260 to 300 grams were randomly divided into five groups(n=12):the sham-operated group(group S);the model con-trol group (group M);propofol group (group P);remifentanil group (group R);propofol combined with remifentanil group (group PR).In group M,P,R,PR,the hepatic arteries and veins of middle and left lobes were occluded for 20 min after 1 w hepatocirrhosis by using four principal factors,and group S went through an open surgery only.In groups P,R,and PR,porpofol (at a rate 20 mg·kg-1 ·h-1 for 1 h)、remifentanil (at a rate 1 μg·kg-1·min-1 for 1 h)and porpofol (at a rate 20 mg·kg-1· h-1 )combined with remifentanil(at a rate 1 μg·kg-1·min-1 for 1 h)was infused iv at 10 min before is-chemia,respectively.In group M,normal saline was infused iv at the same rate.Blood samples were taken at the end of 4 h reperfusion to determine serum AST,ALT activity.Meanwhile liver specimens were collected to assess Bcl-2 and Bax protein expression in liver cell and measuring the apoptosis in-dex(AI)of hepatic cell.The pathological change of liver was also examined.Results Compared with group S,the activity of AST,ALT,the expression of Bcl-2 and Bax and the apoptosis index(AI)of hepatic cell of the other groups all increased significantly(P <0.05);Compared with group M,the expression of Bcl-2 of groups P,R,PR significantly increased,and the activity of AST,ALT,the ex-pression of Bax and the apoptosis index(AI)of hepatic cell significantly decreased(P <0.05 );Com-pared with groups P and R,the expression of Bcl-2 of group PR significantly increased,and the activ-ity of AST,ALT,the expression of Bax and the apoptosis index(AI)of hepatic cell significantly de-creased(P <0.05);Microscopy and scanning electron microscopy showed that,for groups P,R,PR, pathological injury of liver tissue significantly reduced compared with group M.Conclusion Propofol combined with remifentanil can reduce the hepatic ischemia-reperfusion injury in cirrhotic rat by regu-lating Bcl-2 and Bax protein expression and inhibiting apoptosis.The effect is much more enhanced when they are used in combination than individuals.
ABSTRACT
Objective The study was to compare the effect of sufentanil and morphine preconditioning on ischemia /reperfusion-induced ventricular arrhythmias and the expression and distribution of myocardial Cx43 in rats.The regulation mechanisms that how sufentail and morphine lead to the change of Cx43 were also studied.Methods 32 male SD rats were randomly divided into 4 groups:sham operation group (group C),ischemia/reperfusion (group I/R),morphine preconditioning group(group M) and sufentanil preconditioning group(group S),each group had 8 rats.Established myocardial ischemia/reperfusion model,continuous recorded Ⅱ ECG,mean arterial pressure(MAP) and heart rate(HR).The ventricular arrhythmias at the 30 min before reperfusion was observed and the ventricular arrhythmias score of each group was calculated by ECG analysis; expression and distribution of Cx43 protein were observed by immunohistochemical technique.Results Compared with group C,the HR,MAP,RPP of group I/R were decreased obviously (P < 0.05),while the arrhythmia score was significantly higher(P < 0.05).Compared with group I/R,the extent of the declined of HR,MAP,RPP of group M and group S were eased significantly(P < 0.05) and arrhythmia score was significantly lower(P < 0.05).The HR,MAP,RPP of group M and group S are closer(P > 0.05).Compared with the group C,Cx43 expression level in group I/R was significantly reduced (P < 0.05) and the distribution was disordered,while compared with the group I/R,Cx43 expression level in group M and group S were significantly increased (P < 0.05),and its distribution was structured.In group M and group S,Cx43 expression level were closer(P > 0.05) and so as their distribution.Conclusion Sufentanil and morphine could inhibit the reduction of myocardial Cx43 expression level and improve its distribution which could played an important role in anti-arrhythmic during ischemia-reperfusion.
ABSTRACT
Objective To evaluate the effects of amiodarone on connexin43 (Cx43) expression during myocardial ischemia-reperfusion (I/R) in rats.Methods Adult male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:shame operation group (group S),I/R group and amiodarone group (group AM).Myocardial ischemia was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 120 min of reperfusion in I/R and AM groups.Amiodarone 5.0 mg/kg was injected intravenously at 10 min before ischemia followed by infusion at a rate of 0.15 mg· kg-1 · min 1 until the end of reperfusion.Arrhythmia was recorded during reperfusion and scored.At the end of reperfusion,blood samples were taken from the femoral artery for determination of the serum levels of cardiac troponin Ⅰ (cTnI) and creatine kinase isoenzyme-MB (CK-MB).Then the animals were sacrificed and myocardial specimens were removed for determination of the expression of Cx43 protein (by immuno-histochemistry) and mRNA (by RT-PCR) in myocardial tissues.Results Compared with group S,the arrhythmia score and serum levels of CK-MB and cTnl were significantly increased,and the expression of Cx43 protein and mRNA was downregulated in I/R and AM groups (P < 0.05).Compared with group I/R,the arrhythmia score and serum levels of CK-MB and cTnI were significantly decreased,and the expression of Cx43 protein and mRNA was up-regulated in group AM (P < 0.05).Myocardial Cx43 was unevenly distributed in group I/R,while evenly distributed in S and AM groups.Conclusion The mechanism by which amiodarone protects myocardium against I/R-induced arrhythmia is related to inhibition of redistribution of Cx43 and up-regulation of Cx43 expression in rats.
ABSTRACT
Objective To investigate the effects of intrathecal (IT) lidocaine on propofol-induced sedation and content of lidocaine in brain tissues in rats.Methods Twenty male Sprague-Dawley rats,aged 2-3 months,weighing 250-350 g,were equally and randomly assigned to one of four groups:control group (group C),iv lidocaine group (group IV-L),IT normal saline group (group IT-NS) and IT lidocaine group (group IT-L).Groups IT-NS and IT-L received IT normal saline 15μl and 2% lidocaine 15 μl,respectively.Group IV-L received iv 2% lidocaine 15 μl.Propofol was infused starting from 10 min after IT or iv administration.When the eyelash reflex disappeared,the infusion of propofol was stopped and the dose of propofol consumed was recorded.The rats were sacrificed in IT-L and IV-L groups and brains were removed for determination of lidocaine level in brain tissues (by RP-HPLC).Results Compared with groups C,IV-L and IT-NS,the dose of propofol consumed when the eyelash reflex disappeared was significantly decreased in group IT-L (P < 0.05).No significant difference was found in the propofol requirement when the eyelash reflex disappeared between groups C,IV-L and IT-NS and in the content of lidocaine in brain tissues between groups IV-L and IT-L (P > 0.05).Conclusion Sedation induced by lidocaine administered intrathecally is not due to a direct action of lidocaine on the brain in rats.
ABSTRACT
Objective To investigate the effects of remifentanil postconditioning and combined remifentanil-prupofol postconditioning on liver ischemia-reperfusion (I/R) injury in rats.Methods Thirty male SD rats weighing 220-280 g were randomly divided into 5 groups ( n =6 each):group sham operation (group Ⅰ ) ; group I/R (group Ⅱ ) ; group propofol postconditioning (group Ⅲ ) ; group remifentanil postconditioning (group Ⅳ ) and group combined propofol-remifentanil postconditioning (group Ⅴ ).In groups Ⅱ- Ⅴ the hepatic arteries and veins of middle and left were occluded for 30 min.In groups Ⅲ-Ⅴ propofol ( at 30 mg· kg- 1 · h - 1 ) and/or remifentanil (at 1 μg· kg- 1 · min- 1 ) were infused iv at the onset of reperfusion for 1 h.Blood samples were taken at the end of 1 h reperfusion for determination of serum AST,ALT activities and IL-8,IL-10 concentrations.The animals were sacrificed after blood sampling.Liver specimens were obtained for determination of c-fos and c-jun expression in liver cells by immuno-histochemistry and microscopic examination with scanning electron microscope.Results Liver I/R significantly increased serum AST and ALT activities and IL-8 and IL-10 concentrations and c-fos and cjun expression in liver ceils in group Ⅱ as compared with group Ⅰ.The serum AST and ALT activities,IL-8 concentration and the c-fos and c-jun expression in liver cells were significantly lower.and the serum IL-10 concentration was significantly higher in groups Ⅲ- Ⅴ than in group Ⅱ,but there were no significant differences among the groups Ⅲ - Ⅴ.The histo-pathological changes in the liver tissue were significantly attenuated in groups Ⅲ- v as compared with group Ⅱ.Conclusion Postconditioning with remifentanil and/or propofol can attenuate liver I/R injury by inhibiting inflammatory response and apoptosis in the liver cells,but there is no significant difference in the protective effects induced by postconditioning with remifentanil or propofol alone or in combination.
ABSTRACT
Objective To investigate the role of central and peripheral sensitization in remifentanil-induced hyperalgesia in a rat model of inflammatory pain. Methods Twenty-one male SD rats weighing 200-300 g were used in this study. Inflammatory pain was induced by intraplantar injection of 1 % carrageenan 100 fd in the left hindpaw in all animals. The animals were then randomly divided into 3 groups ( n = 7 each): control group (group C) and two remifentanil groups (group R1 , R2) . In R1 and R2 groups remifentanil was infused iv at a rate of 10 and 30 μg-kg-1·min-2 respectively starting from 5 min before till 25 min after carrageenan injection, while in group C normal saline was infused iv instead of remifentanil. Bilateral paw withdrawal threshold to mechanical stimulation with von Frey filament (PWT) was measured before (baseline) and at 1 h, 3 h and 1-7 d after carrageenan injection. Bilateral paw withdrawal latency to noxious thermal stimuli (PWL) was measured before and at 2 h, 4 h and 1-7 d after carrageenan injection. The thickness of the plantar surface of left hindpaw was measured before and at 1 h, 4 h and 1-7 d after carrageenan injection. Results Bilateral PWT was significantly lower at day 1 after carrageenan injection in R, and R2 groups than in group C. The right PWT was significantly lower at 2 d and 4-7 d after carrageenan injection in group R2 than in group R, . There was no significant difference in PWL and thickness of the plantar surface of left hindpaw among the 3 groups. Conclusion Central sensitization is involved in developing and maintaining the remifentanil-induced hyperalgesia in a rat model of inflammatory pain, while peripheral sensitization is not.
ABSTRACT
ObjectiveTo investigate the effect of remifentanil on hepatic ischemia-reperfusion (I/R) injury in rats with liver cirrhosis.MethodsThirty male SD rats weighing 260-300 g were randomly divided into 3 groups (n =10 each):group liver cirrhosis (group C); group liver cirrhosis + hepatic I/R (group I/R) and group remifentanil (group R).Liver cirrhosis was produced in all animals in the 3 goups.I/R injury was induced by 20 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by 4 h reperfusion at 1 week after establishment of hepatic cirrhosis in I/R and R groups.In group R remifentanil was infused iv at 1 μg·kg-1 ·min-1 starting from 10 min before ischemia until the end of 4 h reperfusion.Venous blood samples were taken from inferior vena cava at the end of 4 h reperfusion for measurement of serum ALT and AST activities.The animals were then sacrificed and liver specimens were taken from middle lobe for determination of Bcl-2 and Bax expression (by immuno-histochemistry) and hepatocyte apoptosis (by TUNEL) and microscopic examination.Apoptosis index (percentage of apoptotic cells) was calculated.ResultsI/R significantly increased serum ALT and AST activities,Bax expression and apoptosis index and decreased Bcl-2 expression in group I/R as compared with group C.Remifentanil significantly attenuated the I/R-induced changes in serum ALT and AST activities,Bax and Bcl-2 expression and apoptosis in group R as compared with group I/R.Remifentanil also ameliorated I/R-induced liver damage.ConclusionRemifentanil can auenuate hepatic I/R injury in rats with liver cirrhosis by up-regulating Bcl-2 expression and down-regulating Bax expression and inhibiting apoptosis.