Respiratory mechanics and lung histology in normal rats anesthetized with sevoflurane.

Respiratory system, lung, and chest wall mechanical properties were subdivided into their resistive, elastic, and viscoelastic/inhomogeneous components in normal rats, to define the sites of action of sevoflurane. In addition, we aimed to determine the extent to which pretreatment with atropine modified these parameters. Twenty-four rats were divided into four groups of six animals each: in the P group, rats were sedated (diazepam) and anesthetized with pentobarbital sodium; in the S group, sevoflurane was administered; in the AP and AS groups, atropine was injected 20 min before sedation/anesthesia with pentobarbital and sevoflurane, respectively. Sevoflurane increased lung viscoelastic/inhomogeneous pressures and static elastance compared with rats belonging to the P group. In AS rats, lung static elastance increased in relation to the AP group. In conclusion, sevoflurane anesthesia acted not at the airway level but at the lung periphery, stiffening lung tissues and increasing mechanical inhomogeneities. These findings were supported by the histological demonstration of increased areas of alveolar collapse and hyperinflation. The pretreatment with atropine reduced central and peripheral airway secretion, thus lessening lung inhomogeneities.

Temporal evolution of pneumothorax: respiratory mechanical and histopathological study.

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.