Objective To explore the expression and effect of heme oxygenase-1 ( HO-1) in ventilator-induced lung injury. Methods Twenty-four New Zealand rabbits were randomly assigned to three groups, ie. a conventional ventilation + PEEP group( C group) , a ventilator-induced lung injury group( VILI group) , and a VILI + HO-1 inducer hemin group( Hm group) .Western blot and immunohistochemistry assay were used to investigate the expression of HO-1 protein. Blood gas analysis, lung wet /dry ratio, lunghistopathology and lung injury score were used to evaluate lung injury. Results HO-1 protein expression significantly increased in the VILI group compared with the C group. HO-1 was found mainly in alveolar epithelial cells and vascular endothelial cells, as well as in alveolar macrophages and neutrophils. Compared with the VILI group, HO-1 protein and PaO2 /FiO2 increased, while lung wet/dry ratio and lung injury score decreased in the Hmgroup significantly( P lt;0. 05) . Conclusion High HO-1 expression can alleviate lung injury from large tidal volume ventilation, implying its protective role in lung pathogenesis.
Objective To establish a rabbit model of ventilator-induced lung injury. Methods Fourty healthy New Zealand rabbits were randomly divided into 3 groups: ie. a routine 8 mL/kg tidal volume group( VT8 group) , 25 mL/kg large tidal volume group( VT25 group) , and 40 mL/kg large tidal volume group( VT40 group) . VT25 and VT40 group were further divided into 2 hours and 4 hours ventilation subgroups. Arterial blood gas, lung mechanical force and hemodynamic parameters were monitored. Lungtissue was sampled for evaluate lung wet/dry ratio and lung injury by HE stain. Bronchoalveolar lavage fluid ( BALF) was collected for measurement of protein concentration, total and differential cell counts. Results Compared with VT8 group, lung injury score in both VT40 and VT25 groups were elevated significantly, ofwhich 4 hour VT40 subgroup was the highest. Lung pathology examination of VT40 group revealed apparent alveolar deformation, interstitial and alveolar space exudation, inflammatory cells infiltration, pulmonary consolidation and alveolar hemorrhage. Lung pathology examination of VT25 group showed pulmonary intervalthickening, inflammatory cells infiltration, while alveolar intravasation was mild. Blood gas analysis showed that PaO2 /FiO2 was deteriorated with time in VT25 and VT40 groups, and PaO2 /FiO2 at the 3 hours in VT40 group( lt; 300 mm Hg) had met the acute lung injury standard, while which in VVT25 group was above 300 mmHg. Lung wet/dry ratio, BALF protein concentration, total nucleated cell and neutrophilic leukocyte were elevated in both VT25 and VT40 groups, of which 4 hours VT40 group was the highest. Conclusion Using 4 hours ventilation at a tidal volume of 40 mL/kg can successfully establish the rabbit model of ventilator-induced lung injury.
Objective To investigate the prevalence and predisposing factors of gastroesophageal reflux（GER）in patients with chronic obstructive pulmonary disease（COPD）and its impacts on the frequency of COPD exacerbations.Methods 50 patients with acute exacerbation of COPD were enrolled in the study.All patients filled a modified version of clinically validated standardized Mayo Clinic GER questionnaire.Pulmonary function tests（PFT），body mass index（BMI），serum albumin，and medications were recorded.The patients were divided in to GER group（13 patients with GER symptoms longer than one year and diagnosed GER by gastroscope） and non-GER group（37 patients without GER symptoms）.Results There were no significant differences in the BMI，serum albumin，use of inhaled steroids and theophylline between the two groups.Forced expiratory volume in one second as a percentage of the predicted value（FEV1%pred）（37% vs 38.3%，P=0.608.），residual volume % predicted（123.4 % vs 137.8%，P=0.222），and residual volume to total lung capacity（139.4% vs 141.5%，P=0.798） were not significantly different between the two groups.The number of COPD exacerbations per year was significantly higher in patients with GER compared to patients without GER（4.5 vs 1.3，P=0.006）.Conclusions The severity of airflow obstruction and the hyperinflation is unlikely to contribute to the development of GER.Patients with GER experience significantly more exacerbations per year when compared to patients without GER，suggesting more highlight warrant in treatment of GER in COPD patients.