Objective:To observe clinical therapeutic effect of fasudil hydrochloride in patients with chronic heart failure (CHF).Methods: A total of 134 CHF cases were selected from our department.According to random number table, they were randomly and equally divided into routine treatment group and fasudil group, both groups were treated for three months.Left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDd), left ventricular end-systolic dimension (LVESd), levels of brain natriuretic peptide (BNP), endothelin (ET)-1 and atrial natriuretic peptide (ANP) were compared between two groups before and after treatment.Results: Compared with fasudil group before treatment and routine treatment group after treatment, there were significant reductions in LVEDd [(58.20±8.44) mm, (58.22±10.21)mm vs.(51.24±7.37)mm], LVESd [(47.52±6.51) mm, (47.56±6.54)mm vs.(41.24±5.33)mm], levels of BNP [(381.35±62.48) μg/L, (377.82±61.46) μg/L vs.(294.52±51.33) μg/L], ET-1 [(81.93±13.53) μg/L, (81.32±12.63) μg/L vs.(68.44±11.42) μg/L] and ANP [(215.33±39.72) μg/L, (210.51±36.17) μg/L vs.(172.26±27.54) μg/L], and significant rise in LVEF [(29.69±4.08)%, (29.94±4.25)% vs.(37.47±5.26)%] in fasudil group after three-month treatment, P<0.01 all.Total effective rate of fasudil group was significantly higher than that of routine treatment group (94.0% vs.80.6%, P=0.019).There was no significant difference in incidence rate of adverse reactions between two groups, P>0.05.Conclusion:Fasudil hydrochloride can significantly reduce levels of BNP, ET-1 and ANP, delay ventricular remodeling and improve cardiac function in CHF patients.The therapeutic effect is significant and safety is good.

Objective To evaluate the effects of interleukin-10 and dexamethasone on expression of TNF-? mRNA, IL-1? mRNA, and IL-1ra mRNA in acute lung injury (ALI). Methods A rat model of ALI was reproduced by intratracheal instillation of endotoxin (LPS) with a dose of 10mg/kg. 72 male S-D rats were randomly divided into control group, LPS group, LPS+IL-10 group, and LPS+Dex group, 18 rats in each group (6 rats at 2h, 6h, and 24h respectively). RT-PCR method was used to determine the expression of TNF-? mRNA, IL-1? mRNA, and IL-1ra mRNA in lung tissue. Results In LPS group TNF-? mRNA expression peaked at 2h, then decreased sharply; IL-1? mRNA expression increased markedly at 2h, peaked at 6h, then decreased; IL-1ra mRNA expression increased and peaked at 6h, and remained higher than control group at 24h. Both IL-10 and Dex inhibited TNF-? mRNA and IL-1? mRNA expression, but with no effect on IL-1ra mRNA expression. Pathological examination revealed that IL-10 or Dex attenuated injury to lung parenchyma. Conclusions The up-regulation of expression of both TNF-? mRNA and IL-1? mRNA was much earlier than that of the expression of IL-1ra mRNA, suggesting that there was an imbalance of inflammatory and anti-inflammatory mediators in the early phase of ALI. Both IL-10 and Dex could inhibit the expression of inflammatory mediators and exert no effect on the expression of anti-inflammatory mediators, thus contributing a balance effect between them and relieving ALI in rats.

OBJECTIVE To investigate nosocomial pulmonary infection in elderly patients receiving long-term(at least 30 day) mechanical ventilation. METHODS Retrospective survey was carried out in the aged patients with long-term mechanical ventilation,who admitted from Jan 2002 to Jun 2005.The risk factors of common pneumonia were studied by means of Logistic regression analysis. RESULTS In 69 cases with long-term mechanical ventilation,53 patients were caught common pneumonia(76.81%).Pulmonary tuberculosis and plural tuberculosis were(7(10.14%)) and(1(1.14%)),respectively.Nontuberculous mycobacterial infection was identified in 3 cases(4.35%).There were 8 cases suffered from Pneumocystis carinii pneumonia(11.59%).The length of mechanical ventilation and aspiration seemed to be the important risk factors for the development of common bacterial pneumonia. CONCLUSIONS The most significant preventive measures of common pneumonia include short mechanical ventilation and prevention of aspiration of gastric contents.Mycobacterium tuberculosis,nontuberculous mycobacteria and P.carinii induced pneumonia also should be considered in the elderly with(long-term) mechanical ventilation.

Objective To investigate the cause of pleural effusion in elderly patients on mechanical ventilation, and to analyze the effect of mechanical ventilation on hemodynamics. Methods 100 elderly patients admitted to our hospital from Jan 2002 to Oct 2004 who had received mechanical ventilation were studied retrospectively and logistic regression analysis of risk factors of pleural effusion before and after mechanical ventilation were performed. 8 patients of them were examined by ultrasonic cardiography before and during mechanical ventilation. Results Before mechanical ventilation there were 27 patients complicated with pleural effusion. After mechanical ventilation another 33 patients were showed to develop pleural effusion. Totally 60 mechanical ventilated patients had pleural effusion. The analysis of logistic regression showed that cardiac insufficiency was significantly correlated with pleural fluid in the patients receiving mechanical ventilation. The transmembrane pressure of tricuspid valve was increased during mechanical ventilation. Conclusion Incidence of pleural effusion increased, hemodynamics changed and the transmembrane pressure of tricuspid valve increased with mechanical ventilation in the elderly patients. Cardiac insufficiency was an important risk factor of pleural effusion.

The change of PKC activity and cytosolic free Ca 2+ induced by oxLDL and simvastatin in ASMC were measured by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and flow cytometric analysis loading with the Ca 2+ dye fluo-3/Am, respectively. As a result, oxLDL increased total PKC activity in a dose-dependent manner with phase peaking at 14 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic [Ca 2+]i responses including rapid initial transient phase and sustained phase. Removal of extracellular Ca 2+did not inhibit the rapid phase of oxLDL-induced rise in [Ca 2+]i, but abolished the sustained phase of [Ca 2+]i in response to oxLDL. Activity of PKC was markedly decreased and simvastatin did not impair the initial peak in response to oxLDL but significantly reduced the subsequent plateau phase when simvastatin was added. The results suggested that oxLDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca 2+in ASMC. The rapid initial transient phase was due to the mobilization of [Ca 2+]i from intracellular Ca 2+ pool and the sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may contribute to the changes of intracellular Ca 2+.

Objective： To investigate the effect of oxLDL and VitE on the expression of CD40 and CD40 ligand(CD40L) in cultured human monoc ytes. Methods： The expression of CD40 and CD40L on monocytes su rface were measured by indirect immunorescence technique in combination with flo w cytometry. Results： Low concentration of oxLDL（≤200 μg/L） significantly increased the expression of CD40 and CD40L in a dose and time dep endent manner. High concentration (>200 μg/L）of oxLDL markedly reduced the exp ression of CD40 and CD40L. When VitE was added, it significantly reduced the ex pression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose-depe ndent manner. Conclusion：It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the for mation of atherosclerosis. Antioxidan VitE can partially inhibit the high expres sion of CD40 and CD40L on monocytes surface induced by oxLDL.

AIM: To investigate whether human umbilical vein endothelial cells and human atherosclerotic plaque lesions can coexpress CD40 and CD40 ligand . METHODS: The expression of CD40 and its ligand CD40L on human endothelia cells were measured by fluorescence microscope , flow cytometry(FCM), reverse transcription PCR(RT-PCR) and Western blotting, respectively. Both CD40 and CD40L expression in atheroma plaques were determined by immunohistochemistry. RESULTS: Cultured human endothelial cells constitutively coexpressed CD40 and CD40L in mRNA and protein levels. Stimulation with interleukin-1?, interleukin-6, tumor necrosis factor-? and interferon-? increased expression of CD40 and CD40L on endothelial cells . Human atherosclerotic lesions( n =6) showed coexpression of immunoreactive CD40 and CD40L. However, no expression of CD40 and CD40L in nonatherosclerotic human arteries. CD40L mainly expressed on the shoulder and base of the plaque. But CD40 was widespreadly expressed in plaque. CONCLUSION: Our results demonstrated that CD40 and CD40L coexpressed on human umbilical vein endothelial cells and in human atherosclerotic plaque lesions. These findings suggest a previously unsuspected role for CD40-CD40L interactions in atherosclerosis.

Objective To evaluate the performance of homocysteine(Hcy)test kit produced by a domestic company and to inves-tigate its feasibility in clinical application.Methods A series of methodological evaluation experiments including the accuracy,re-peatability,stability and linear range of the Hcy reagent kit were carried out on the Olympus Au640 biochemistry analyzer.Results The experiments showed that the relative biases of detection results of normal value quality control serum and pathological value quality control serum were 0.2% and 4.9%,respectively,which were far less than 15% of the reagent instruction.The intra-assay coefficients of variation(CV)of normal and pathological quality control serum were 2.6% and 2.3% respectively,which were less than 5% of the reagent instruction.While the inter-assay CV of normal and pathological quality control serum were 4.4% and 4.1% respectively,which were less than 10% of the reagent instruction.The experiments for the linear range evaluation showed that R 2 was 0.997 in the concentration range of 0 -66 μmol/L,which suggested that the correlation between expected value and measured value was very well.Otherwise,the slope rate b1 of 0.979 9 and the intercept b0 of 0.151 8 were both showed that the de-tection results of Hcy reagent were linear in the concentration of 0-66 μmol/L.Conclusion The performance of Hcy kit produced by a domestic company is very good in the performance indexes of accuracy,repeatability,stability,and linear range and suitable for the clinical application.

Objective To investigate the feasibility and effects of whole-procedure seamless nursing intervention during regional collaborative treatment of patients with acute coronary syndrome.Methods Nursing intervention was performed on pre-hospital collaboration,transfer collaboration and catheter room collaboration during regional collaborative treatment of patients with ACS.Treatment time point,therapeutic effects and major hospitalization indicators were compared before(the control group) and after(the experimental group) implementation of nursing intervention.Results There were significant differences in mean FMC-to-B time,D-to-B time,referral time,obtaining informed consent time,mortality,LVEF and LVED between two groups(P＜0.05).There were significant differences in days of hospitalization,expenditures,percentage of consumables,percentage of medication,and in-hospital mortality between two groups (P＜0.05).Conclusion Whole-procedure nursing intervention can reduce time of regional collaborative treatment of patients with acute coronary syndrome,improve prognosis,decrease financial burden and increase efficiency of ACS treatment.

200 ?g/L)of oxLDL markedly reduced the expression of CD40 and CD40L. When VitE was added, it significantly reduced the expression of CD40 and CD40L on monocytes surface induced by oxLDL in a dose dependent manner. Conclusion:It is an important mechanism that the high expression of CD40 and CD40L induced by oxLDL may be contributed to the formation of atherosclerosis. Antioxidan VitE can partially inhibit the high expression of CD40 and CD40L on monocytes surface induced by oxLDL. [