[The expression of thrombospondin-1 in serum and pulmonary arterioles of hypoxic pulmonary hypertension rats].

OBJECTIVE: To investigate the expression of thrombospondin-1 (TSP-1) in serum and pulmonary arterioles of rats with hypoxic pulmonary hypertension. METHODS: Twenty male Wistar rats were divided into two groups and exposed to air and isobaric hypoxia for 3 weeks respectively. The mean pulmonary artery pressure (mPAP) was measured by right cardiac catheterization. The rates of wall thickness/external diameter (WT%) and wall area/total vascular area (WA%) were calculated. The TSP-1 level in serum was measured by enzyme-linked immunosorbent assay. TSP-1 mRNA expression in lung tissue was evaluated by quantitative PCR. RESULTS: The pulmonary artery pressure increased in the hypoxia exposed rats. The chronic hypoxia also elicited the thicking of the wall and the narrowing of the lumen of pulmonary arterioles. It led to the increases of pulmonary artery pressure, the index of right ventricular hypertrophy [RV/(LV+S)], WA% and WT% compared to the controls [mPAP:(2.86 +/- 0.39) kPa vs. (1.35 +/- 40.28) kPa; RV/(LV+ S): (43.53 +/- 3.38)% vs. (23.68 +/- 3.48)%; WT%: (35.24 +/- 11.20)% vs. (23.63 +/- 9.74)%; WA%: (55.09 +/- 12.38)% vs. (41.62 +/- 12.83)% respectively, P<0.05]. In hypoxic group, the expression of TSP-1 mRNA in the lung was significantly up-regulated, the expression level of TSP-1 in serum was higher than that in control group (P<0.01). Linear correlation analysis showed that TSP-1 mRNA was positively associated with WT%, WA% and mPAP (r= 0.748, 0.686, 0.942 respectively, P<0.05). CONCLUSION: The TSP-1 may play an important role in the pathogenesis process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.

[Expression of thrombospondin-1 in the lung of hypoxic pulmonary hypertension rats].

OBJECTIVE: To investigate the expression of thrombospondin-1(TSP-1) in the lung of hypoxia-induced pulmonary hypertension rats. METHODS: Thirty male Wistar rats were divided into two groups, pulmonary hypertension group and control group. The mice in experimental group were exposed to isobaric hypoxia for 3 weeks, and those in control group were exposed to air. The pulmonary artery pressure was measured by right cardiac catheterization. The expression of TSP-1 and TGF-beta1 in the lungs of rats were measured by immunohistochemical staining. The histological sections of the lungs were examined using a computerized image analyzer. RESULTS: After the induction of hypoxia for 3 weeks, the rats had pulmonary artery pressure increased with the thickening of the wall and the narrowing of the lumen of pulmonary arterioles. In the experimental group, the mean pulmonary artery pressure (mPAP) was (2.86 +/- 0.39) kPa, the index of right ventricular hypertrophy RV/(LV+S) was (43.53 +/- 3.38)%, the ratio of vascular wall thickness/vascular external diameter (WA%) was (55.09 +/- 12.38)%, and the ratio of vascular wall area/total vascular area (WT%) was (35.24 +/- 11.2)%, which all were significantly increased in comparison with those of control group [mPAP (1.35 +/- 0.28) kPa, RV/(LV+S) (23.68 +/- 3.48)%, WT% (23.63 +/- 9.74)%, WA% (41.62 +/- 12.83)%, respectively. P < 0.05). The positive staining of TSP-1 (1.32 +/- 0.04 vs. 0.96 +/- 0.03) and TGF-beta1 (1.38 +/- 0.05 vs. 1.04 +/- 0.04) in the wall of pulmonary arteriole of the rats exposed to hypoxia were significantly stronger than those of control rats (P < 0.01). CONCLUSION: The expression of TSP-1 appears to be increased in hypoxic pulmonary hypertension rats, which may contribute to the pathogenesis of hypoxic pulmonary vascular remodeling.

[The effect of nasal continuous positive airway pressure on endothelial function in obstructive sleep apnea-hypopnea syndrome with coronary heart disease].

OBJECTIVE: To study the association between the indices of endothelial function in obstruction sleep apnea-hypopnea syndrome (OSAHS) and coronary heart disease (CHD) and the effect of nasal continuous positive airway pressure (nCPAP) on the combination of OSAHS and CHD. METHODS: A total of 80 subjects were prospectively recruited into four groups including control, OSAHS, CHD, OSAHS with CHD groups, with 20 subjects each. The indices of sleep apnea, serum nitric oxide (NO), and plasma endothelial-1 (ET-1) were measured. The changes of concentration of ET-1 and NO were compared before and after nCPAP therapy. The associations between ET-1 and NO and MSpO2, CT90 were analyzed. RESULTS: (1) Multi-variable logistic analysis showed that OSAHS was one of the risk factors for CHD (OR = 0.511). (2) Compared with the control subjects and CHD group, there were significantly higher values of CT90, concentrations of ET-1 and lower values of MSpO2, concentrations of NO in both OSAHS and OSAHS with CHD groups (P < 0.01). There were no significant difference in sleep apnea indices between OSAHS and OSAHS with CHD groups (P > 0.05). However, in the group of OSAHS with CHD, the plasma ET-1 was significantly higher, whereas the serum NO was significantly lower than that in the group of OSAHS alone (P < 0.01). (3) The concentration of serum NO in the group of OSAHS was positively correlated with MSpO2 (r = 0.519, P < 0.05) and inversely correlated with CT90 (r = -0.529, P < 0.05). In addition, the concentration of plasma ET-1 was inversely correlated with MSpO2 (r = -0.457, P < 0.05) and positively correlated with CT90 (r = 0.476, P < 0.05). (4) In the groups of OSAHS and OSAHS with CHD, MSpO2, NO and NO/ET-1 after nCPAP therapy were higher than those before therapy, while CT90 and ET-1 were lower than those before therapy (P < 0.01). CONCLUSIONS: OSAHS is one of the risk factors for CHD. Endothelial function was significantly impaired in OSAHS patients, and more severe in patients with OSAHS with CHD. The impairment of endothelial function may be one of the main mechanisms for the development or deterioration of CHD in OSAHS patients. The vascular endothelial dysfunction can be ameliorated by nCPAP treatment, which is correlated with improvement of nocturnal hypoxemia.

[Corticosteroid therapy and changes in chest radiogram in five patients with severe acute respiratory syndrome].

OBJECTIVE: To investigate the relationship between corticosteroid therapy and kinetic changes in chest X-ray in five patients with severe acute respiratory syndrome (SARS). METHODS: With the identical underlying therapy (levofloxacin or ceftriaxone and macrolide), intravenous methylprednisolone was given at 80 mg twice a day in five patients, and its effect on the development of chest radiogram was observed. RESULTS: Chest X-rays radiogram showed significant changes until peak stage (4-12 days) with the same doses of methylprednisolone, but it was dissolved consistently afterwards. CONCLUSION: It is appeared that corticosteroid therapy has no marked effect on the development of chest radiogram in patients with SARS. It might indicate there is self-limited in course of SARS.

[Effect of adenoviral E1A-involved apoptosis of rat alveolar epithelial cells and human lung adenocarcinoma epithelial cell line].

AIM: The relationship between latent adenovirus infection and apoptosis of airway epithelial cell have not been well documented.We want to illustrating the roles of adenovirus E1A protein on the apoptotic alveolar epithelial in response to TNF-alpha. METHODS: The expression vector for expressing adenovirus E1A protein was transfected into CCL149 and A549 cell respectively. Cell stably expressing E1A protein were selected by G418 resistance.All G418-resistant clones were indentified by RT-PCR and immunocytochemistry. The rate of apoptosis were measured by Hoeschest 33 258 and flow cytometry respectively. The apoptotic rate in response to 30 microg/L TNF-alpha was compared between E1A-positive clones and control clones both in A549 and CCL149. RESULTS: The rates of apoptosis were (2.63+/-0.8)%, (25.38+/-0.9)% respectively in E1A-positive CCL149 cell and (0.62+/- 0.3)%, (6.08+/-0.2)% respectively in E1A-negative CCL149 cell. The rates of apoptosis were (2.63+/-0.8)%, (25.38+/-0.9)% respectively in E1A-positive A549 cell and (0.62+/- 0.3)%, (6.08+/-0.2)% respectively in E1A-negative A549 cell. The rate of apoptosis were increased in E1A-positive cells compared with control with or without TNF-alpha stimulation. CONCLUSION: E1A sensitizes cell to TNF-alpha induced apoptosis of A549 cell and CCL149 cell.