ABSTRACT
Aim To investigate the relationship between monocyte chemoattractant protein-1(MCP-1) and pulmonary artery hypertension after acute pulmonary thromboembolism(PTE), and to explore the effects and mechanisms of resveratrol with MCP-1 in the acute PTE as well.Methods The acute PTE model of Sprague-Dawley rats was replicated using self-thrombosis.The rats were randomly divided into five groups(Normal, Solvent, acute PTE, antibody Cl142, and resveratrol), and 1h, 4h, 8h and 3 points were observed in each group.A model of acute PTE was established by infusion of an autologous blood clot into the pulmonary artery through a polyethylene catheter.Resveratrol or Cl142, dissolved in 1％ dimethyl sulfoxide(DMSO), was administered to the animals through caudalvein 1 h prior to the beginning of acute PTE modeling.Rats in normal control group and solvent control group were injected with normal saline and 1％ DMSO respectively.The mean pulmonary artery pressure(MPAP) and the mRNA and protein expression of MCP-1 were measured at each time point.Results ① The acute PTE group MPAP, MCP-1 mRNA and protein expression were significantly higher than those of the control group(P<0.05) at the same time;② The resveratrol group′s MPAP and MCP-1 mRNA, protein expression were significantly lower than those of the acute PTE group(P<0.05) at the same time;③ The Cl142 group MPAP and MCP-1 mRNA, protein expression were markedly reduced in the acute PTE group(P<0.05) at the same time.Conclusions The large expression of MCP-1 after acute PTE is involved in the formation of pulmonary hypertension after acute PTE.Resveratrol can reduce the pressure of pulmonary artery after acute PTE by down-regulating the MCP-1 expression.
ABSTRACT
Objective To investigate the effect of bilevel positive airway pressure (BiPAP) ventilation on N terminal pro-brain natriuretic peptide (N proBNP) in patients with chronic pulmonary heart disease (CPHD) and hypercapnic respiratory failure.Methods Eighty patients with CPHD and hypercapnic respiratory failure were randomized into the conventional group (n=40) and BiPAP ventilation group (n=40).The COPD assessment test (CAT) score,APACHE Ⅱ score,arterial blood gas were measured and plasma level of N proBNP was detected by electrochemiluminescence immunoassay before and 120 h after treatment.The correlations of plasma N-proBNP levels with CAT scores,APACHE Ⅱ scores,levels of PaO2 and PaCO2 were analyzed.Results The plasma NT-proBNP level had positive correlations with PaCO2 level (r=0.539,P =0.003),CAT score (r＝0.506,P＝0.002,APACHEⅡ score (r=0.603,P=0.003),and had negative correlation with PaO2 level (r=-0.465,P=0.014) in the patients with CPHD and hypercapnic respiratory failure before treatment.Compared with pre-treatment,the scores of CAT and APACHE Ⅱ,the levels of PaO2 and PaCO2 were significantly improved 120 h after treatment.The improvements in APACHE Ⅱ,PaO2 and PaCO2 were more obviously significant in BiPAP ventilation group than in conventional group (t=5.55,5.92,4.12,respectively,P=0.002,0.001 and 0.000).The plasma levels of NT proBNP in both conventional and BiPAP ventilation groups were significantly descended 120 h after treatment than pre-treatment [(341.2±107.6) ng/L vs.(823.8±149.0) ng/L,(273.3±82.2) ng/L vs.(832.7± 163.0) ng/L,t=21.72,28.19,both P＜0.001],and the decrease of NT-proBNP level was more significantly in BiPAP ventilation group than in conventional group (t=4.17,P=0.002).Conclusions Plasma NT-proBNP level can reflect the severity of chronic pulmonary heart disease combined with hypercapnic respiratory failure.BiPAP ventilation can decrease the plasma level of NT proBNP in patients with CPHD and hypercapnic respiratory failure,which is an effective treatment for chronic pulmonary heart disease combined with hypercapnic respiratory failure.