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This study have analyzed the pulmonary function in an experimental model of acute lung injury, induced by the Crotalus durissus cascavella venom (C. d. cascavella) (3.0 μg/kg - i.p), in pulmonary mechanic and histology at 1 h, 3 h, 6 h, 12 h and 24 h after inoculation. The C. d. cascavella venom led to an increase in Newtonian Resistance (R N ), Tissue Resistance (G) and Tissue Elastance (H) in all groups when compared to the control, particularly at 12 h and 24 h. The Histeresivity (η) increased 6 h, 12 h and 24 h after inoculation. There was a decrease in Static Compliance (C ST ) at 6 h, 12 h and 24 h and inspiratory capacity (IC) at 3 h, 6 h, 12 h and 24 h. C. d. cascavella venom showed significant morphological changes such as atelectasis, emphysema, hemorrhage, polymorphonuclear inflammatory infiltrate, edema and congestion. After a challenge with methacholine (MCh), R N demonstrated significant changes at 6, 12 and 24 h. This venom caused mechanical and histopathological changes in the lung tissue; however, its mechanisms of action need further studies in order to better elucidate the morphofunctional lesions., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The aim of this study was to evaluate the effect of a chemical sclerosing agent, aluminum hydroxide, on pleural remodeling and on respiratory mechanics in rats. Saline (2 mL) or aluminum hydroxide [2 mL (0.15 g/mL)] was instilled intrapleurally in anesthetized male rats. The animals were studied 7 or 30 days after the instillation. Respiratory system, lung, and chest wall elastic, resistive, and viscoelastic/inhomogeneous pressures were measured by the end-inflation occlusion method. We studied the pleural remodeling process by means of semiquantitative analysis of the induced inflammation and quantitative analysis of the collagen extracellular matrix component. The effects on the underlying lung were analyzed morphometrically. Chest wall elastic and viscoelastic pressures increased after aluminum hydroxide instillation independent of time after instillation. Pleural inflammation was observed 7 days after instillation, while pleural adherence with a marked increase in the type I/type III collagen ratio was present 30 days after instillation. Histological examination demonstrated no differences in lung parenchyma among the groups. In conclusion, the present model describes the establishment of pleurodesis by aluminum hydroxide, which thwarts the normal chest wall mechanical profile without inducing any changes in the underlying lungs. The results were disclosed by both mechanical and morphological evaluation of the pleural remodeling.

Respiratory mechanics, chest wall configuration, and lung morphometry were determined in rats before and at 30 (PTX.30) and 60 (PTX.60) min after pneumothorax induction (intrathoracic injection of 8 ml of room air; 50% collapse). Pneumothorax increased respiratory system and lung elastances and viscoelastic/inhomogeneous pressures in both groups, but respiratory system and lung resistive pressures increased only in PTX.60 group. Antero-posterior diameters at the third intercostal space and xiphoid levels, circumference at xiphoid level, and thoracic cephalo-caudal diameter increased significantly after pneumothorax induction independently of temporal evolution. In both groups lung collapse, hyperinflation, and interstitial and alveolar edema were present. Additionally, in PTX.60 group the central airways calibre diminished in relation to PTX.30. In conclusion pneumothorax yields changes in respiratory system and lung elastic and viscoelastic parameters, which are related to alveolar collapse and edema, respectively. Temporal evolution of pneumothorax also leads to changes in lung resistive pressure, probably because of airway narrowing.