Resictive breathing induced lung injury

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

Prediction of dysnatremias in critically ill patients based on the law of conservation of mass. Comparison of existing formulae.

BACKGROUND:We aimed to examine the predictive value of a novel mathematical formula based on the law of conservation of mass in calculating sodium changes in intensive care unit patients and compare its performance with previously published formulae. METHODS:178 patients were enrolled from 01/2010 to 10/2013. Plasma and urine were collected in two consecutive 8-hour intervals and the sodium was measured. The predicted sodium concentration was calculated based on previous equations and our formula. The two 8-hour period (epoch 1 and 2) results were compared. Variability of predicted values among the measured range of serum sodium levels were provided by Bland-Altman plots with bias and precision statistics. Comparison of the results was performed with the statistical model of the Percentage Similarity. RESULTS:47.19% patients had dysnatremias. The bias ± SD with 95% limits of agreement for sodium levels were -1.395±3.491 for epoch 1 and -1.623 ±11.1 for epoch 2 period. Bland-Altman analysis for the epoch 1 study period had the following results: -0.8079±3.447 for Adrogué-Madias, 0.56±9.687 for Barsoum-Levine, 0.1412±3.824 for EFWC and 0.294±4.789 for Kurtz-Nguyen formula. The mean similarity, SD and coefficient variation for the methods compared with the measured sodium are: 99.56%, 3.873, 3.89% epoch 1, 99.56%, 1.255, 1.26% for epoch 2, 99.77%, 1.245, 1.26% for Adrogue-Madias, 100.1%, 1.337, 1.34% for Barsoum-Levine, 100.1%, 1.704, 1.7% for Nguyen, 100.1%, 1.370, 1.37% for ECFW formula. CONCLUSIONS:The law of conservation of mass can be successfully applied for the prediction of sodium changes in critically ill patients

Automated detection, segmentation and measurement of major vessels and the trachea in CT pulmonary angiography

Mediastinal structure measurements are important for the radiologist's review of computed tomography pulmonary angiography (CTPA) examinations. In the reporting process, radiologists make measurements of diameters, volumes, and organ densities for image quality assessment and risk stratification. However, manual measurement of these features is time consuming. Here, we sought to develop a time-saving automated algorithm that can accurately detect, segment and measure mediastinal structures in routine clinical CTPA examinations. In this study, 700 CTPA examinations collected and annotated. Of these, a training set of 180 examinations were used to develop a fully automated deterministic algorithm. On the test set of 520 examinations, two radiologists validated the detection and segmentation performance quantitatively, and ground truth was annotated to validate the measurement performance. External validation was performed in 47 CTPAs from two independent datasets. The system had 86-100% detection and segmentation accuracy in the different tasks. The automatic measurements correlated well to those of the radiologist (Pearson's r 0.68-0.99). Taken together, the fully automated algorithm accurately detected, segmented, and measured mediastinal structures in routine CTPA examinations having an adequate representation of common artifacts and medical conditions

Angiopoietin-1 Protects against Airway Inflammation and Hyperreactivity in Asthma

Rationale: The angiopoietins (Ang) comprise a family of growth factors mainly known for their role in blood vessel formation and remodeling. The best-studied member, Ang-1, exhibits antiapoptotic and antiinflammatory effects. Although the involvement of Ang-1 in angiogenesis is well recognized, little information exists about its role in respiratory physiology and disease. On the basis of its ability to inhibit vascular permeability, adhesion molecule expression, and cytokine production, we hypothesized that Ang-1 administration might exert a protective role in asthma. Objectives: To determine changes in the expression of Ang and to assess the ability of Ang-1 to prevent the histologic, biochemical, and functional changes observed in an animal model of asthma. Methods: To test our hypothesis, a model of allergic airway disease that develops after ovalbumin (OVA) sensitization and challenge was used. Measurements and Main Results: Ang-1 expression was reduced at the mRNA and protein levels in lung tissue of mice sensitized and challenged with OVA, leading to reduced Tie2 phosphorylation. Intranasal Ang-1 treatment prevented the OVA-induced eosinophilic lung infiltration, attenuated the increase in IL-5 and IL-13, and reduced eotaxin and vascular cell adhesion molecule 1 expression. These antiinflammatory actions of Ang-1 coincided with higher levels of IκB and decreased nuclear factor-κB binding activity. More importantly, Ang-1 reversed the OVA-induced increase in tissue resistance and elastance, improving lung function. Conclusions: We conclude that Ang-1 levels are decreased in asthma and that administration of Ang-1 might be of therapeutic value because it prevents the increased responsiveness of the airways to constrictors and ameliorates inflammation