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Objective To investigate the clinical therapeutic effect of Shenqi Fuzheng injection for treatment of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).Methods A prospective clinical study was conducted. Fifty-eight consecutive patients with AECOPD were admitted in Departments of Respiratory Disease and Critical Care Medicine in Zhuozhou City Hospital of Hebei Province from January 2012 to December 2013. They were randomly divided into western medicine (WM) control group (28 cases, the routine treatment of WM) and integrated traditional Chinese medicine (TCM) with WM group (30 cases, on the basis of conventional therapy, Shenqi Fuzheng injection 250 mL intravenous drip was given once a day for a therapeutic course of 10 days). The duration of mechanical ventilation, the successful rate of weaning from ventilator, the rate of using ventilator again after weaning, the length of stay in intensive care unit (ICU), and mortality were recorded respectively in the two groups. Before and after treatment, the arterial blood gas analysis, acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score, clinical pulmonary infection score (CPIS), pulmonary function and dyspnea score were evaluated. Results Compared with the WM control group, the duration of mechanical ventilation (hours: 104±16 vs. 125±24) and the length of stay in ICU (days: 6.3±2.1 vs. 7.2±3.6) were significantly shorter, the rate of successful weaning from ventilator was obviously higher [73.3% (22/30) vs. 60.7% (17/28)], and the rate of using ventilator again after weaning was remarkably lower [13.3% (4/30) vs. 28.6% (8/28)] in the combined TCM and WM group, the differences between the two groups being statistically significant (allP 0.05). Compared with those before treatment, the pH value, arterial partial pressure of oxygen (PaO2), forced expiratory volume in 1 second (FEV1), forced vital capacity(FVC) and the ratio of FEV1/FVC were all significantly higher in the two groups after treatment, while the partial pressure of arterial carbon dioxide (PaCO2), APACHE Ⅱ score, CPIS score, residual volume/total lung capacity (RV/TLC), and the dyspnea score were all lower in the two groups after treatment, the more obvious changes in levels being after 10 days of treatment in combined TCM and WM group [pH: 7.44±0.04 vs. 7.40±0.08, PaCO2 (mmHg, 1 mmHg = 0.133 kPa): 59.1±11.9 vs. 68.1±12.4, PaO2 (mmHg): 70.5±6.9 vs. 65.1±7.4, APACHE Ⅱ score: 14.5±4.2 vs. 17.4±2.2, CPIS score: 5.3±2.4 vs. 7.6±1.4, FEV1 (L): 1.60±0.47 vs. 1.54±0.34, FEV1/FVC: (65.33±2.65)% vs. (62.00±3.25)%, FVC (L): 1.72±0.21 vs. 1.66±0.21, RV/TLC: (42.13±1.67)% vs. (43.12±0.95)%, dyspnea scores: 1.71±0.54 vs. 2.32±0.65, allP < 0.05].Conclusion Shenqi Fuzheng injection possesses certain clinical value in treatment of patients with AECOPD, as it can obviously improve the pulmonary function and the data of arterial blood gas analyses, and effectively relieve the clinical symptoms.
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The effects of testosterone on norepinephrine release were investigated in the isolated rat hearts. Sprague-Dawley male rats (n=120) were randomized to testosterone and control groups. The rats in testosterone group were perfused with modified Krebs-Henseleit buffer containing different concentrations of testosterone (0.1, 1.0, 10.0, and 100.0 nmol/L, respectively). Myocardial ischemia was induced by globally stopping the perfusion flow. Exocytotic norepinephrine release was induced by electrical field stimulation at 5 V (effective voltage) and 6 Hz (pulse width of 2 ms) for 1 min. The overflow of norepinephrine was determined by high pressure liquid chromatography and electrochemical detection (HPLC-EC). Following acute ischemia, testosterone (1.0, 10.0 and 100.0 nmol/L) significantly reduced norepinephrine release (P0.05). Electrical stimulation of the ventricle evoked norepinepherine release, and this was diminished by the perfusion with testosterone at the concentrations of 1.0, 10.0 and 100.0 nmol/L (P<0.01). It is suggested that testosterone suppresses ischemia- and electrical stimulation-induced norepinepherine release in the isolated rat hearts.
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Objective To examine the clinical effects of intravenous lyophilize recombinant human brain natriuretic peptide (rhBNP) in patients with refractory heart failure caused by coronary artery disease.Methods Seven patients with refractory heart failure caused by coronary artery disease were treated with rhBNP.The rhBNP nea grade,symptoms and signs,24 hours urine output,heart rate,blood pressure and central venous pressure were evaluated at 0,15,30 min and 1,2,4,8,12,24,and 48 h.Serum potassium,sodium,creatinine and plasma BNP before and after treatment were measured.Results After rhBNP therapy,dyspnea grade were improved in 5 patients.Symptoms and signs got better in 6 patients.Systolic blood pressure at 15 min of treatment distolic blood pressure was decreased slightly from (112.00±10.42) mm Hg to (105.14±7.76) mm Hg (P＜0.05) and became (108.71±6.63)mm Hg at 30 rain which was the same with that before treatment.There was no statistical significance in heart beat[ ( 88.57±16.92 ) vs.( 86.00±16.21 ) ] beat/min,serum sodium [ ( 133.57±5,38 ) mmol/Lvs.( 133.57±8.16) mmol/L ],serum potassium [ (3.83±0.37) mmol/L vs.(4.19±0.58 ) mmol/L ],ereatinine [ (93.11±27.90) μmol/L vs ( 123.01±93.01 ) μmol/L ] before and after treatment,and BNP[ ( 1218.43±847.83) vs.(1433.71±676.08)ng/L] before treatment and at24 h treatment,as well as urine output [(2329±1573 ) vs.(2126±1074) ml ] ( P ＞ 0.05 ).Urine output was increased during the treatment,but the usage of diuretic was remarkably decreased.Central venous pressure was gradually decreased from 30 rain to 48 h( P ＜ 0.05 ).Condusion rhBNP can decrease central venous pressure and increase urine output with exerts little side effects on electrolytes and renal function.Therefore rhBNP has positive clinical effects on refractory heart failure which is caused by coronary artery disease.
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Objective To investigate the effect of 9-cis retinoid acid(c-RA),a retinoid X receptor(RXR)agonist,on hydrogen peroxide(H2O2)induced apoptosis in cultured rat neonatal cardiomyoeytes,and to explore the mechanism.Method Cultured cardiomyocpes were randomly divided into three groups:normal group treated with vehicle(N group),H2O2 group treated with 100 μmol/L H2O2(H group),and c-RA group pretreated with 100nmol/L c-RA(H+R group).Cell viability was detected by MTT.Morphological changes of apoptotic cardiomyocytes were observed by Hoechst 33258 staining under fluorescence microscope.The apoptotic rate was determined by flow cytometry.Mitochondrial membrane potential(△(ψ)m)was measured by JC-1 dye.Cellular reactive oxygen species(ROS)production was detected by CM-H2DCFDA fluorescent probe.All measurement data wIe expressed as(x±s),and statistically analyzed using one-way ANOVA analysis and Dunnett test.Differences were considered significant when P was＜0.05.Results Treatment with c-RA significantly enhanced cell viability,reduced apoptosis ratio,stabled mitoehondrial membrane potential and reduced level of cellular reactive oxygen species.Conclusions RXR agonist c-RA inhibits H2O2-induced myocyte apoptosis in cultured rat neonatal cardiomyocytes,which may be related to alleviate oxidative stress injury.
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Objective: To investigate the effects of grasp seed procyanidins(GSP,原青花素) on lipopolysaccharide(LPS)induced acute lung injury(ALI) in rats with renal function damage and the related possible molecular mechanisms.Methods: The homogenates of lung and kidney were prepared and venous blood were collected at 6 hours after injection of LPS and medicine.The changes of contents of creatinine(Cr),blood urea nitrogen(BUN),lactic acid(Lac) and nitric oxide(NO) in the blood were measured.The enzyme linked immunosorbent assay(ELISA) was used to measure the levels of tumor necrosis factor?(TNF-?),interleukin-1?(IL-1?),monocyte chemoattractant protein-1(MCP-1) and IL-6 in the serum,lung and renal cortex tissue homogenate in various groups.The histopathological changes of lung tissues were observed.The pulmonary vascular permeability and the lung wet/dry(W/D) weight ratio were determined;the malonaldehyde(MDA) content,Na+K+-ATPase,superoxide dismutase(SOD),myeloperoxidase(MPO) and glutathion peroxidase(GSH-Px) activities in lung and renal tissues were also determined.Changes of mitogen activated protein kinase(MAPKs) were detected by Western blotting,and the combination activity of nuclear factor-?B(NF-?B) to DNA was detected by electrophoretic mobility shift assay (EMSA) in lung tissues.Results: ①Compared with the normal rats in control group,the lungs of the rats in LPS treatment group and GSP group had significant hyperemia and spotted hemorrhage.The inflammatory granulocyte infiltration,diffuse alveolar septum thickening and spotted hemorrhage were observed in the pathological examinations,while in LPS plus GSP group the above mentioned pathological changes were milder.②Compared with control group,the lung W/D and pulmonary vascular permeability were much higher in the LPS treatment groups(P
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AIM:To investigate the effects of silymarin on lipopolysaccharide(LPS)-induced acute lung injury in rats and its possible molecular mechanisms.METHODS: Fifty-eight male SD rats,weighting 230-250 g,were divided into four groups randomly: normal control(n=12);acute lung injury group(n=15),receiving intravenous LPS(O55∶B5,5 mg/kg);silymarin alone group(50 mg/kg,n=15);intervention group(n=16,receiving silymarin 50 mg/kg and LPS 5 mg/kg).The specimens were collected 6 hours later.The following changes,including blood gas analysis,the lung wet/dry weight ratio,the pulmonary vascular permeability,histological manifestations,lung tissue myeloperoxidase activity,the levels of TNF-?,IL-1?,MCP-1 and SOD,GSH-Px as well as malonaldehyde and conjugated diene in plasma and lung tissue,were observed.RESULTS: Compared with control group,the lungs of the rats in LPS treatment group showed significant hyperemia and spotted hemorrhage.The inflammatory granulocyte infiltrating,diffused alveolar septum thickening and spotted hemorrhage were observed in pathological examinations.The lung wet/dry weight ratio and Evans blue content(per gram) increased significantly after LPS treatment.The myeloperoxidase activity in plasma and lung tissue,the levels of TNF-?,IL-1?,MCP-1 and SOD,GSH-Px as well as malonaldehyde and conjugated diene were increased significantly in LPS treatment group.However,in intervention groups,all the above-mentioned measurements were reversed significantly by silymarin treatment compared with LPS treatment group.CONCLUSION: Silymarin may decrease inflammatory reaction and oxidative stress,and further decrease lung damage induced by LPS in rats,all indicating protection of silymarin against acute lung injury.