Objective To observe the inhibitory effect of xiaoaiping injection and octreotide on H22 tumor-bearing mice and find the best drug concentration,then to explore its mechanism.Methods Establish a mouse H22 subcutaneous tumor model.After tumor the experiment animals were divided into normal control group,model group,Xiaoaiping low,medium and high dose group,octreotide group,and the group of XAP low,medium and high dose groups were combined with OCT.Calculate the tumor's volume and draw the tumor growth curve.Intraperitoneal injection for 14 days,Inhibitory rate was calculated; To observe its pathological changes by light microscope; The ratio.of CD3 + NK1.1-T cells,CD3-NK1.1 + NKcells,CD3 + NK1.1 + NK-Tcells in peripheral blood were measured by flow cytometry.Results Compared with the control group,H22 liver cancer in different treatment group had a certain inhibition effect on growth,The inhibitory effect of the combination group was better than single-agent group,High-dose Xiaoaiping + octreotide was best,Tumor model group compared with normal control group,The ratio of T cells,NK cells and NKT cells was significantly lower(P ＜0.05) ; T cells,NK cells and NKT cells after treatment in each group had some enhancement,High-dose Xiaoaiping + octreotide was the most obvious,the ratio of T cells,NK cells and NKT cells of the combination group was significantly more than the single-drug group and the same concentration of octreotide monotherapy Xiaoaiping group(P ＜ 0.05).Conclusion High-dose Xiaoaiping + octreotide is the best drug for the inhibitory drug concentration.The inhibition of tumor growth may pass to improve the tumorbearing mice with immune status and enhance the body's anti-tumor capacity.

Objective To investigate the difference among neonatal rat models of hypoxia-ischemia induced white matter injury of brain by three different methods and to provide theory basis on choosing the proper animal model for deep study on white matter injury of premature infants.Methods Three different hypoxia-ischemia methods were applied to induce brain white matter injury model of Wistar rats of postnatal 3rd day which were left carotid artery ligation followed by 6％ oxygen for 30 minutes and for 4 hours respectively,and bilateral carotid artery ligation followed by 8％ oxygen for 30 minutes.Compared brain pathological results of rats in different groups,changes in white matter of brain by glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) immunostaining,and changes in time of opening eyes and eyes appearance.Results Left carotid artery ligation followed by 6％ oxygen for 30 minutes resulted in sparse and vague periventricular white matter without necrotic lesions,and the degree of GFAP intensity [(5 021.63 ± 358.92) OD] increase and MBP intensity [(18 488.63 ± 1 822.62) OD] decrease were lowest (P ＜ 0.000 1),as well as the delay of opening time of the left eye.Left carotid artery ligation followed by 6％ oxygen for 4 hours resulted in necrotic lesions of periventricular white matter,with the degree of GFAP intensity [(6 069.13 ± 458.61) OD] and MBP intensity [(15 003.38 ± 1 559.11) OD],and also the delay of opening time of the left eye.Bilateral carotid artery ligation followed by 8％ oxygen for 30 minutes caused cystic necrosis of bilateral periventricular white matters,and the degree of GFAP intensity [(6 194.50 ±432.69) OD] increase and MBP intensity [(10 119.35 ± 735.16) OD] decrease of the left side were highest(P ＜ 0.000 1),as well as the delay of opening time and cataract in both eyes.Conclusion Left carotid artery ligation followed by 6％ oxygen for 30 minutes is more suitable for investigating mild brain white matter injury.Left carotid artery ligation followed by 6％ oxygen for 4 hours and bilateral carotid artery ligation followed by 8％ oxygen for 30 minutes are more proper for the investigation of severe periventricular leukemacia cases.

AIM\ To study the protective mechanism of ligustrazine(LT), shenmai injection(SI), combination of ligustrazine and shenmai injection (LSI) to injury of kidney after brain ischemia reperfusion in aged rats from the free radical change. METHODS Aged rats (more than 20 months) were divided into model group (Aged model), control group(Aged control), nimotop group(NG), ligustrazine group(LG), shenmai injection group(SIG) and LSI group(LSG). The following items was measured in aged rats with 60 min reperfusion after 30 min brain ischemia: the content of creatinine(Cr), urea nitrogen(BUN), MDA and the activitiy of superoxide dismutase(SOD). RESULTS The distinct pathological and functional injury in the kidney was found in the models, and this change was alleviated in each treatment group. The increase of MDA content in the models kidney tissue was obvious than that in the controls. The MDA level in the LG and the SIG was decreased. CONCLUSION The kidney injury after brain ischemia reperfusion in aged rats is correlated with the injury of free radical. LT, SI ,LSI and nimotop alleviate this injury. LT and SI restraine the injury of lipid peroxidation, this may be one of the mechanisms of restraining kidney injury after brain ischemia reperfusion.

Objective:To investigate the effects of dexmedetomidine on perioperative cardiac adverse events in elderly patients with coronary heart disease.Methods:Sixty elderly patients,who were diagnosed as coronary heart disease and underwent gastric cancer operation,were randomly divided into 2 groups (n=30):the dexmedetomidine group (Dex group) and the control group.In the Dex group,dexmedetomidine was administered intravenously at 0.5 μtg/(kg.h) after a bolus infusion at 0.5 μg/kg for 10 min before anesthesia induction.In the control group,equal volume of normal saline was infused instead of dexmedetomidine.The 2 groups received the same anesthesia treatment.The venous bloods were collected at the preoperative 0 h and postoperative 24 h.The concentrations of cardiac troponin (cTnⅠ),N-terminal pro-brain natriuretic peptide (NT-proBNP) and hypersensitive C-reactive protein (hs-CRP) were determined.The ECG was monitored at the above time and the postoperative incidence of cardiac adverse events was recorded.Results:The levels of cTnⅠ,NT-proBNP and hs-CRP in serum were elevated in the 2 groups after the operation.Compared with the control group,the levels of cTnⅠ,NT-proBNP and hs-CRP were significantly decreased in the Dex group (P＜0.05).Compared with the control group,the incidence ofbradycardia were significantly increased,while the myocardial ischemia and tachycardia were significantly decreased in the Dex group during the operation (P＜0.05);the incidence of silent myocardial ischemia and arrhythmia was significantly reduced at 3 days after operation in the Dex group (P＜0.05).Conclusion:Dexmedetomidine could decrease the incidence of cardiac adverse events in elderly patients with coronary heart disease.

AIM: To study the mechanism of myocardial injury after brain ischemia-reperfusion in aged rats from the changes in Dopamine (DA), Noradrenalin (NE), Epinephrine(E) and Neuropeptide Y(NPY).METHODS: Young (5 months) and aged (20 months or more) rats were divided into model groups and normal control groups, respectively. We observed the following items in rats with 60 minute reperfusion after 30 minute brain ischemia: the pathological changed of myocardium, the activities of lactic dehydrrogenase(LDH), creatine phosphokinase(CPK), the contents of NE, DA, E, NPY. RESULTS:The CPK and LDH activities in the young model rats were higher than those in the young control rats was higher than that in the young control rats (P＜0.05). The serum CPK activity in the aged control rats was higher than that in the young control rats (P＜0.05). The myocardial CPK activity was higher in the aged model rats compared with the young molel rats (P＜0.05) and was higher in aged control rats compared with the young control rats (P＜0.01). The myocardial LDH activity was lower in the aged control rats than that in the young control rats (P＜0.05) and aged model rats (P＜0.01). The serum NE level, the level of NE and DA in the hypothalamus were higher obviously than those in the young control rats. The serum NE contents in the two model groups (young and aged) were higher respectively than the two control rats (young and aged). The following items’ contents were higher in the aged model rats than in the young model rats: serum NE, serum E, hypothalamus NE. The hypothalamus NE and E content was lower in the aged model rats than in te aged control rats. NPY level in the brain tissue was lower in the aged control rats than that in the young control rats and aged model rats (P＜0.05).CONCLUSION: The myocardial injury after brain ischemia-reperfusion was concerned with the enhanced excitability of sympathetic-adrenal system, espectially in the aged rats. However, the change in myocardial enzyme was not serious in the aged rats compared with young rats.

AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na＋-K＋-ATPase and Ca2＋-ATPase in model group was decreased. Contrast to the model group, the activity of Na＋-K＋-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2＋-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na＋-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2＋-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.

AIM: To study the mechanism of brain ischemia-reperfusion injury from ATPase activity and free radical metabolism in aged rats. METHODS: The young rats (5 months) and the aged rats (more than 20 months) were divided into young control group(YCG), young model group(YMG), aged control group(ACG) and aged model group(AMG). The ATPase and SOD activities and the contents of MDA, Ca 2+ , Na + and K + were measured in the rats with 30 min brain ischemia followed by 60 min reperfusion. RESULTS: The Ca 2+ content in the AMG was higher than that in the YMG and the ACG. The Na +-K +-ATPase activity in the ACG was lower than that in the YCG,was lower in the AMG than that in the YMG . The Ca 2+ -ATPase activities in the YCG was higher than that in the ACG, was lower in the AMG than that in the YMG and was higher than the ACG's. The serum and brain tissue SOD activities in the ACG was lower than that in the YCG, was lower in the AMG than YMG 's. The serum and brain tissue MDA/SOD ratio in the AMG was higher than that in the ACG. CONCLUSION: The brain tissue ischemia- reperfusion injury was related with calcium overload and free radical injury. The pathological changes were obvious and had some characteristics in the aged rats compared with the young rats because of the brain tissue aging changes in ATPase,calcium content and free radical metabolism in the aged rats.

Objective To summarize the clinical features and etiology of cerebral infarction in children.Methods The clinical data of 47 children with cerebral infarction who were hospitalized in Shengjing Hospital of China Medical University from Jan 2009 to Jul 2011 were analyzed retrospectively.Results There were 30 boys and 17 girls in all the 47 children.The median age of onset was 3.1 years(ranged from 2 months to 11 years old).Among 47 cases,the common neurological manifestations included limb paralysis in 32 cases(68.1％ ),central facial paralysis in 15 cases(31.9％ ),convulsion in 12 cases(25.5％ ),disturbance of consciousness in 10 cases(21.3％ ),and language disorders in 10 cases(21.3％ ).Among 47 cases,31 cases had basal ganglia infarction with neuronal imaging( CT or MRI),of whom 4 cases accompanied with other location infarction.Several lobes of infarction in 5 cases,hemispheric infarction in 3 cases,parietal infarction in 2 cases,frontal lobe infarction in 2 cases,temporal lobe infarction in 2 cases,and thalamic infarction in 2 cases.Nineteen cases were carried out blood vessel imageology examination,11 cases showed abnormality,the most common affected cerebral blood vessel were middle cerebral artery(5 cases).The common causes of 47 cases were trauma ( 19 cases,40.4％ ),infection( 12 cases,25.5％ ) and moyamoya disease (5 cases,10.6％ ).Ten children (21.3％) had no identifiable cause.Conclusion The common period of cerebral infarction is in infancy.The most frequent neurological symptom is hemiplegia.The most common region of infarction is in basal ganglia with neuronal imaging.The common causes of cerebral infarction are trauma,infection and moyamoya disease.

Objective To observe the clinical efficacy and adverse reaction of Chuanxiongqingnaokeli for children with migraine. Methods One hundred children patients with migraine were randomly divided into treatment group( n = 50 ) and control group( n = 50 ). Patients in treatment group were given Chuanxiongqingnaokeli,10 g/once,and three times one day,while in control group were given Flunarizine Hydrochloride Capsules,2. 5 mg/once,and who's body mass ﹥50 kg with 5. 0 mg/once,and one times each night. Three months as one course of treatment,and compared the efficacy of two groups after tree course of treatment. Results The hemodynamics of two groups all decreased after treatment compared with before treatment,but ACA,MCA,PCABA and VA in treatment group(( 81. 10 ± 11. 95 ),( 93. 3 ± 14. 16 ),( 70. 2 ± 11. 57),(70. 6 ± 13. 02),(65. 5 ± 12. 6)cm/s respectively)decreased more significantly than that of control group(( 104. 2 ± 12. 63 ),( 116. 2 ± 15. 82 ),( 93. 5 ± 11. 91 ),( 93. 5 ± 12. 71 ),87. 4 ± 12. 92 ) cm/s respectively),and the differences were significant( P﹤0. 05). The headache frequency and duration in treatment group were(1. 0 ± 0. 6)and(3. 3 ± 1. 0),less than that of control group((2. 3 ± 0. 9)and(5. 6 ± 1. 7);t= -3. 345,-3. 269;P﹤0. 05). The total effective rate in treatment group was 90. 0%(45/50),higher than that of control group(74. 0%(37/50);χ2 =4. 336,P﹤0. 05). There was no severe adverse reaction in both two groups. Conclusion The Chuanxiongqingnaokeli is safe and effective for treatment of children with migraine.

Objective To evaluate the effect of obesity on the potency of propofol for sedation.Methods Sixty patients of both sexes, aged 35-55 yr, of American Society of Anesthesiologists physical status Ⅰ or Ⅱ , scheduled for elective operation under general anesthesia, were enrolled in the study.The patients were divided into 2 groups (n=30 each) according to the body mass index (BMI) : normal body weight (BMI ＜ 25 kg/m2) group (group C) and obesity (BMI 30-40 kg/m2) group (group O).No patients received premedication.Propofol was given by target-controlled infusion.The initial target plasma concentration of propofol was set at 1.2 μg/ml.After the target concentration was steadily maintained for 30 s, it was increased in 0.3 μg/ml increment until the patients lost consciousness (OAA/S score =1).The target plasma concentration of propofol was recorded during each period.The median effective concentration (EC50) and 95％ confidence interval of propofol for loss of consciousness was calculated using probit analysis.Results The EC50 and 95％ confidence interval of propofol for loss of consciousness were 3.82 (3.73-3.90) and 3.29 (3.20-3.37) μg/ml in group C and group O, respectively.Compared with group C, the EC50 was significantly decreased in group O (P＜0.05).Conclusion Obesity can enhance the potency of propofol for sedation.