Objective: To investigate the effect of different concentrations of dextrose transfusion on cerebral glucose metabolism in pediatric neurosurgical operations. Methods: Sixty anesthetized children undergoing selective cerebral tumor resection were randomly divided into three groups: Ringer lactate solution group (A, n = 20), 2.5% dextrose lactated Ringer's solution group(B, n = 20), 1% dextrose lactated Ringer's solution group (C, n = 20). All the hemodynamic data were recorded during anesthesia. The values of blood glucose and lactic acid were collected before intubation(T_a), 2 hours after opening cerebral dura mater (T_b) and the end of operation (T_c). The catheters for microdialysis were punctured into normal brain tissue. The contents of glucose and lactic acid were determined in the collected intercellular fluid by biochemical analysis instruments at T_A and T_B respectively. Results: There were no differences in heart rate(HR), mean arterial pressure(MAP) and arterial oxygen saturation (SpO_2) among three groups(P > 0.05). There were no differences in blood glucose at T_a between three groups(P > 0.05). The values of blood glucose at T_b and T_c were B group＞C group＞A group(P < 0.05). The values of blood glucose were higher at T_b and T_c than that of T_a in three groups(P < 0.05). There were no differences in blood lactic acid among three groups(P > 0.05). There were no significant differences in values of glucose and lactic acid in the collected intercellular fluid among three groups(P > 0.05). Conclusion: Transfusion of Ringer lactate solution or low concentration dextrose solution will increase blood glucose in pediatric neurosurgical operations, but still in the normal range, which has a little influence on blood lactic acid, glucose and lactic acid in brain intercellular fluid. It is a safe choice during neurosurgical operation.

OBJECTIVETo investigate the effect of tanshinone II(A) on the expression of different components in the renin-angiotensin system of left ventricles of renal hypertensive rats.

METHODThe renal hypertension model was established in rats by the two-kidney-one-clip (2K1C) method. In the experiment, all of the rats were randomly divided into four groups (n = 15 per group) before the operation: the sham-operated (Sham) group, the hypertensive model (Model) group, the low-dose tanshinone II(A) group and the high-dose tanshinone II(A) group. At 5 week after the renal artery narrowing, the third and fourth groups were administered with 35 mg kg(-1) x d(-1) and 70 mg x kg(-1) x d(-1) of tanshinone II(A), respectively. The blood pressure in rats was determined by the standard tail-cuff method in each week after the operation. After the drug treatment for 8 weeks, all the rats were put to death, and their left ventricles were separated to determine the ratio of left ventricle weight to body weight (LVW/BW), the myocardial collagen content, and the expressions of different components in myocardial RAS, including angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin 1-type receptor (AT1R), Mas receptor mRNA expression and angiotensin II (Ang II) and angiotensin (1-7) [Ang (1-7)] content.

RESULTCompared with the sham group, the hypertensive model group exhibited a markable increase in the content of Ang II and Ang (1-7) and the mRNA expressions of ACE, ACE2, AT1R and Mas (P < 0.01). However, the treatment with tanshinone II(A) showed the does dependence, inhibited left ventricle hypertrophy, decreased myocardial Ang II content and the mRNA expression of ACE and AT, R in renal hypertensive rats (P < 0. 01) , further increased the myocardial Ang (1-7) content and the mRNA expression of ACE2 and Mas (P < 0.01) , but without any change in the blood pressure of hypertensive rats.

CONCLUSIONThe treatment with tanshinone II(A) could inhibit left ventricle hypertrophy of renal hypertensive rats. Its mechanism may be partially related to the expression of different components in the renin-angiotensin system for regulating myocardial tissues.

Angiotensin I ; genetics ; metabolism ; Angiotensin II ; genetics ; metabolism ; Animals ; Blood Pressure ; drug effects ; Diterpenes, Abietane ; administration & dosage ; Heart Ventricles ; drug effects ; metabolism ; Humans ; Hypertension ; drug therapy ; genetics ; metabolism ; physiopathology ; Male ; Peptide Fragments ; genetics ; metabolism ; Peptidyl-Dipeptidase A ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Renin ; genetics ; metabolism ; Renin-Angiotensin System ; drug effects

Anthracosis ; diagnosis ; Diagnostic Errors ; Humans ; Lung Diseases ; diagnosis ; Male ; Middle Aged ; Pulmonary Artery

ObjectiveTo assess the degree of pain in elderly patients with mechanical ventilation in ICU using critical-care pain observation tool(CPOT) and to choose the correct sedative and analgesic method.Methods 110 elderly patients in ICU after neurosurgery were divided into three assessment stages,every stage had two record points and total six points (T1-T6):the first stage (intubation and unconsciousness,T1-T2),the second stage (intubation and consciousness,T3T4 ) and the third stage(extubation and consciousness,T5-T6 ).Among them T1,T3and T5were nonnocuity assessment points of every stage,while T2,T4 and T6 were nocuity assessment points of every stage.The assessment time was one minute at every point.After recorded at every point in second and third stages,patients were asked to use the pain intensity descriptive scale (PIDS) themselves.CPOT,heart rate and mean arterial pressure (MAP) from T1 to T6 were recorded as well as PIDS from T3 to T6 in second and third stages.Results In the three stages,CPOT〔(26.8 vs.0.54,3.36 vs.1.20,2.78 vs.0.68) scores〕,HR〔(95 vs.85,94 vs.82,94 vs.84)beat/min〕 and MAP〔(95 vs.85,95 vs.87,94 vs.87)mm Hg〕 at T2,T4and T6 were higher than T1 (t=-42.89,-55.95,-55.38),T3 (t =- 5.52,- 11.33,- 11.78) and T5 ( t =- 5.54,- 9.95,- 11.33 ) ( P＜ 0.05 ).The PIDS at T4 and T6were higher than at T3and T5in the second and third stages 〔(2.52 vs.1.69,2.12 vs.1.44)scores〕 (P＜0.05).The correlation coefficient between CPOT and PIDS at T3 and T4 in the second stage were 0.49 and 0.58,respectively (P＜0.05),and between CPOT and PIDS at T5 and T6 were 0.52 and 0.59 in the third stage,respectively (P ＜ 0.05),and they both reached moderate correlation.ConclusionsCPOT may be an effective way to assess the degree of pain in elderly patients with mechanical ventilation at present.

Aged ; Aged, 80 and over ; Alanine Transaminase ; blood ; Bilirubin ; blood ; Choledochostomy ; methods ; Common Bile Duct ; surgery ; Common Bile Duct Neoplasms ; complications ; Drainage ; Female ; Follow-Up Studies ; Humans ; Jaundice, Obstructive ; blood ; etiology ; surgery ; Jejunum ; surgery ; Male ; Middle Aged ; Pancreatic Neoplasms ; complications ; Survival Rate ; gamma-Glutamyltransferase ; blood

Adult ; Aged ; Botulinum Toxins, Type A ; therapeutic use ; Dysphonia ; therapy ; Female ; Humans ; Laryngoscopy ; Male ; Middle Aged

Objective To investigate the effects of ketamine on anoxia-reoxygenation(A/R)induced glutamate release from cerebral cortex neurons.Methods Primary cultured neurons obtained from cerebral cortex of fetal Wistar rats(16-18 d)were randomly divided into 3 groups:Ⅰcontrol group;ⅡA/R group andⅢketamine pretreatment+I/R group.The control group was not subjected to A/R while A/R group was exposed to anoxic air(95% N_2+5% CO_2)for 5 h followed by 24 h reoxygenation.In groupⅢdifferent doses of ketamine were added to the culture media before anoxia and the final ketamine concentrations were 1,20 and 100?mol?L~(-1) respectively.The extracellular glutamate concentration was detected at the end of 24 h reoxygenation.Results The extracellular glutamate concentration was significantly higher after 24 h reoxygenation in A/R group than in control group.Ketamine 20 and 100?mol?L~(-1) significantly inhibited glutamate release from the neurons induced by A/R in a dose-dependent manner.Conclusion Ketamine can inhibit glutamate release from neurons induced by A/R in a dose-dependent manner.

Objective To investigate the effects of hyperbaric oxygenation(HBO)therapy on serum con- centrations of soluble intercellular adhesion molecule-1(slCAM-1),soluble vascular cell adhesion molecule-1(sV- CAM-1),soluble E-selectin(sE-selectin)and matrix metalloproteinase-9(MMP-9)in patients with aeute cerebral infarction and their clinical implications.Methods One hundred and twelve cases of cerehral infarction in the ca- rotid artery system were assigned into two groups.Patients in the routine treatment group(RT group,n=62)were treated with routine clinical treatment regime,whereas those in the HBO group(n=50)were treated with H BO ther- apy in additioo to routine clinical treatment.Thirty age- and sex-matched normal subjects were recruited and served as controls.The serum concentrations of sICAM-1,sVCAM-1,sE-selectin and MMP-9 were measured hy using ELISA method before and 10 days after treatment.The assessment of neurological deficits using National Institutes of Health Stroke Scale(NIHSS)score was conducted before treatment,and at 10 and 30 days after treatment,and the therapeutic efficacy was evaluated.Results The concentrations of sICAM-1,sVCAM-1,sE-selectin and MMP-9 of the patients were significantly higher than those of the control subjects.These parameters were all decreased signifi- cantly after treatment in the two patient groups.Moreover,these parameters were lower in the HBO group than those in the RT group after treatment.The NIHSS scores of HBO group were significantly lower than that of the RT group at the 30th clay post-treatment.The effective rate of HBO group was higher than that of RT group.Conclusion HBO therapy can decrease the serum levels of sICAM-1,sVCAM-1,sE-seleetin and MMP-9,which might be one of the mechanisms of HBO in the treatment of cerebral infarction.

Objective To explore the extent of lung injury induced by hyperoxia,and the activity of ubiquitin-proteasome pathway(UPP) in pathophysiological progress of lung tissue in early stages.Methods Adopted completely random design,20 SD rats were divided into hyperoxia group and air control group.For the air control group,the oxygen concentration exiting the cages was analyzed with oxygen monitor and oxygen concentration remained at 210 mL/L for 72 hours;while in the hyperoxia group,the condition changed into high-density oxygen(950 mL/L) for 72 hours to estimate the hyperoxia lung injury in rats model.The contents linked morphology as pathological classification in gross finding,pathological score of lung injury and the index of pneumonedema-the ratio of moist to dry weight of lungs were mea-sured.The expressions of ubiquitin protein and the activity of proteasome 20 S and the active statement of ubiquitin-proteasome pathway were detected by immunohistochemistry and Western blot methods.Results 1.The hyperoxia lung injury rat model was successfully duplicated.2.In hyperoxia group,pulmonary edema with increased ratio of moist to dry weight of lungs could be found(P=0).3.Macroscopic observation: bright red and full-stacked lung tissue,foliated or local hemorrhage on the surface,but little pleural effusion was observed in hyperoxia group.There was statistical significance of pathological classification in gross finding between hyperoxia group and air control group(P=0.005).Light microscope observation:swelled alveolar epithelium,widened alveoli wall,capillary engorgement and telangiectasis,obvious edema in interstitial tissue of pulmonary aveolus and alveolar space,increased inflammatory cells were observed in hyperoxia group.The findings of pathological score of lung injury indicated more serious injure than control group(P=0).4.The increased expression of ubiquitin protein in lung tissue was discoved by using immunohistochemistry and Western blot findings after hyperoxia exposure 72 hours.(P=0).5.The acti-vity of proteasomes 20 S in hyperoxia group was higher than that in control group(P=0).Conclusions The mainly pathological changes of lung are generated through hyperoxic exposure for 72 hours,including alveolar epithelial cell and vascular endothelial cell injury diffusely,inflammatory cell infiltration and pulmonary edema.Active the ubiquitin-proteasome pathway is connected with the pathophysiological process of lung injury in the initial stages of hyperoxia-exposure.

Objective To investigate the protective effects of the ubiquitin proteasome inhibitor MG-132 on p38 signaling pathway and apoptosis in lung injury induced by hyperoxia. Methods Twenty-six SD rats were randomly divided into 4 groups: normal control group(n=5),MG-132 control group(n=5),hyperoxia group(n=8) and MG-132 hyperoxia group(n=8).Hyperoxia lung injury rat models were established,and proteasome inhibitor(0.5 mg/kg) was intraperitoneally injected in control group and MG-132 hyperoxia group once daily.The resected lungs were histopathologically examined,and cell apoptosis and expression of ubiquitin and p38 were detected by TUNEL and immunohistochemistry,respectively.Results After hyperoxia exposure,there were edema and inflammatory cell infiltration in the lung tissues of SD rats.The apoptosis index and expression of p38MAPK of hyperoxia group were higher than those of normal control group and MG-132 hyperoxia group(P