Role of angiotensin II type 2 receptor during electrophysiological remodeling of left ventricular hypertrophic myocardium in spontaneously hypertensive rats.

The objective was to investigate the role of angiotensin II type 2 receptor during electrophysiological remodeling of left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHRs). A total of 36, aged 10 weeks, male SHRs were divided into three groups: control, valsartan, and valsartan + PD123319 groups (n = 12 in each). The systolic blood pressure, left ventricular mass index, ventricular effective refractory period, and ventricular fibrillation threshold (VFT) were also measured after 8 weeks. At the same time, INa, ICaL, Ito, and membrane capacitance were measured in left ventricular myocytes by whole-cell patch-clamp. The VFT of valsartan was higher than that of control (valsartan vs. CONTROL: 17.4 ± 0.6 mA vs. 15.8 ± 0.5 mA, P < .05). The VFT of valsartan was higher than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: 17.4 ± 0.6 mA vs. 16.6 ± 0.9 mA, P < .05). The density of Ito of valsartan was higher than that of control (valsartan vs. CONTROL: 14.7 ± 0.42 pA/pF vs. 11.2 ± 0.15 pA/pF, P < .05). The density of Ito of valsartan was higher than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: 14.7 ± 0.42 pA/pF vs. 13.6 ± 0.30 pA/pF, P < .05). The density of ICaL of valsartan was lower than that of control (valsartan vs. CONTROL: -4.6 ± 0.2 pA/pF vs. -6.9 ± 0.1 pA/pF, P < .05). The density of ICaL of valsartan was lower than that of valsartan + PD123319 (valsartan vs. valsartan + PD123319: -4.6 ± 0.2 pA/pF vs. -5.4 ± 0.1 pA/pF, P < .05). These results demonstrated that the stimulation of angiotensin II type 2 receptor improved electrophysiological remodeling of left ventricular hypertrophic myocardium in SHR.

[The relationship of peroxisome proliferator activated receptor γ ligands activity in nucleated cell and interleukin-6 level in septic rats].

OBJECTIVE: To observe the relationship between activity of peroxisome proliferator activated receptor γ (PPARγ) in nucleated cell and level of pro-inflammatory mediator interleukin-6 (IL-6) in plasma of rats with sepsis. METHODS: According to the random number table, 90 male Sprague-Dawley (SD) rats were randomly divided into three groups, namely control group, sham operation group and sepsis group. Each group was further divided into three subgroups according to postoperative time points, i.e. 12, 24 and 48-hour subgroups. Each subgroup consisted of 10 rats. Sepsis was reproduced by cecal ligation and puncture (CLP). The PPARγ activity in nucleated cells and IL-6 level in plasma were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The PPARγ activity in nucleated cells was significantly decreased at 12, 24 and 48 hours in sepsis group (A value: 0.279±0.004, 0.264±0.009, 0.245±0.012) compared with control group (0.292±0.007, 0.293±0.004, 0.293±0.005) and sham operation group (0.295±0.008, 0.295±0.006, 0.294±0.007), while the IL-6 level was significantly increased in sepsis group (ng/L: 365.25±15.53, 507.16±20.86, 437.89±25.09) compared with control group (43.54±11.10, 48.82±10.62, 42.96±9.52) and sham operation group (42.43±6.77, 40.32±6.48, 44.10±9.36, all P<0.05). When septic condition became worse, the PPARγ activity in nucleated cells of sepsis group lowered, and IL-6 level was gradually elevated after operation, reaching the peak at 24 hours, and then gradually lowered, and the difference of the value between any two time points was all statistically significant (all P<0.05). There was a negative correlation between the PPARγ activity in nucleated cells and IL-6 level in 12-hour subgroup of sepsis group (r=-0.703, P=0.023). CONCLUSION: In septic rats, the PPARγ activity in nucleated cells was lowered while the pro-inflammatory mediator IL-6 level in plasma elevated, and there was a negative correlation between PPARγ activity and IL-6 level.

Role of TNF-α, sTNF-R55 and sTNF-R75 in inflammation of acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Although some recent studies have demonstrated the important role of tumor necrosis factor-α (TNF-α) and soluble TNF receptors (sTNF-R) in inflammation of chronic obstructive pulmonary disease, the exact roles of TNF-α and sTNF-R as well as their interaction remained unclear. OBJECTIVES: To study changes in levels of systemic and airway local TNF-α and sTNF-R (sTNF-R55, sTNF-R75) in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD), and clarify the relationship between these mediators and airflow limitation in AECOPD patients. METHODS: TNF-α, sTNF-R55 and sTNF-R75 levels in induced sputum and plasma as well as lung functions were examined in 48 AECOPD patients before and after treatment. Samples from 28 healthy volunteers served as controls. RESULTS: Compared to healthycontrols, both pre- and posttreatment levels of TNF-α, sTNF-R55 and sTNF-R75 in induced sputum and plasma of COPD patients were higher. In patients with AECOPD, posttreatment TNF-α levels significantly decreased compared to pretreatment levels (0.6 ± 0.46 vs. 0.82 ± 0.35 µg/l in plasma, p < 0.01; 0.48 ± 0.27 vs. 0.82 ± 0.34 µg/l in sputum, p < 0.001). While posttreatment sTNF-R55 and sTNF-R75 levels increased in both kinds of samples, mediator levels in plasma and lung functions were unrelated (p > 0.05). sTNF-R55 and sTNF-R75 levels in induced sputum were positively correlated with lung functions (p < 0.05), while TNF-α levels were negatively correlated with forced expiratory volume in 1 s (FEV1) and the ratio of FEV1 to FEV1 predicted value. CONCLUSIONS: Inflammatory and anti-inflammatory mediators were imbalanced in the airways of AECOPD patients. It was local inflammation but not systemic inflammation that was closely related to airflow limitation.

[Analysis of the status of diagnosis of acute pulmonary embolism and a study of further strategy to improve the diagnostic level].

OBJECTIVE: To analyze the present status of diagnosis of pulmonary embolism (PE) by analyzing the clinical data of patients admitted during last 10 years to our hospital, in order to look for a significant diagnostic strategy to improve the diagnostic level. METHODS: The data of patients diagnosed to have PE in last 10 years were analyzed. In the last 5 months, the patients suspected to have PE were diagnosed by a comprehensive approach including clinical manifestations, lung scan and/or spirals computer tomography (SCT) in our emergency department. RESULTS: The diagnostic rate, the final diagnostic rate within 3 days and the diagnostic rate by lung scan or/and SCT were all higher in the last 3 months than ever. The proportions of angiograms and the overall 3-month PE risk were 2.8% and 0. CONCLUSION: The comprehensive approach which includes clinical manifestations, lung scan and/or SCT can obviously improve the diagnostic level of PE.