Βλάβη πνεύμονος συνέπεια εργώδους αναπνοής

Abstract

Rationale Resistive breathing is associated with large negative intrathoracic pressures. Increased mechanical stress induces highpermeability pulmonary edema and lung inflammation. Objectives To determine the effects of resistive breathing on the healthy lung. Methods Anesthetized rats breathed through a two-way nonrebreathing valve. The inspiratory line was connected to a resistance setting peak inspiratory tracheal pressure at 50% of maximum (inspiratory resistive breathing), while 100% oxygen was supplied to prevent hypoxemia. Quietly breathing animals (100% oxygen) served as controls. Lung injury was evaluated after 3 and 6 hours of resistive breathing. Measurements and Main Results: After both 3 and 6 hours of resistive breathing, lung permeability was increased, as assessed by 99mTcdiethylenetriaminepentaacetic acid scintigraphy and Evans blue dye extravasation. Tissue elasticity, measured on the basis of static pressure–volume curves and by the lowfrequency forced oscillation technique, was also increased. After both 3 and 6 hours of resistive breathing, gravimetric measurements revealed the presence of pulmonary edema and analysis of bronchoalveolar lavage showed increased total protein content, whereas the total cell count was elevated only after 6 hours of resistive breathing. Cytokine levels were assessed in bronchoalveolar lavage fluid and lung tissue by ELISA and were increased after 6 hours compared with controls. Western blot analysis showed early activation of Src kinase via phosphorylation (at 30 min), and Erk1/2 and IkBa (nuclear factorkB inhibitor) were phosphorylated at 3 and 6 hours. Pathology revealed the presence of lung injury after resistive breathing. Conclusions Resistive breathing induces acute lung injury and inflammation.