Alternating ventilation in a rat model of increased abdominal pressure.

During alternating ventilation (AV) one lung is inflating while the other is deflating. Considering the possible respiratory and hemodynamic advantages of AV, we investigated its effects during increased intra-abdominal pressure (IAP=10 mmHg). In Sprague-Dawley rats (n=6, 270-375g) the main bronchi were independently cannulated, and respiratory mechanics determined while animals underwent different ventilatory patterns: synchronic ventilation without increased IAP (SV-0), elevated IAP during SV (SV-10), and AV with elevated IAP (AV-10). Thirty-three other animals (SV-0, n=10; SV-10, n=11 and AV-10, n=12) were ventilated during 3h. Mean arterial pressure (MAP), and lung histology were assessed. Increased IAP resulted in significantly higher elastances (p<0.001), being AV-10 lower than SV-10 (p<0.020). SV-10 showed higher central venous pressure (p<0.003) than S-0; no change was observed in AV-10. Wet/dry lung weight ratio was lower in AV-10 than SV-10 (p=0.009). Application of AV reduced hemodynamic and lung impairments induced by increased IAP during SV.

Influence of lung mechanical properties and alveolar architecture on the pathogenesis of ischemia-reperfusion injury.

We tested the hypothesis that lung preservation techniques disarrange lung architecture, increase pulmonary impedance and lead to ischemia-reperfusion injury, which can be prevented by re-establishment of optimal lung geometry. In the first phase, fresh, cold ischemic, preserved lungs insufflated to total lung capacity (TLC) and preserved lungs ventilated with tidal volume prior to reperfusion were submitted to a 60-min ex-vivo reperfusion to evaluate the gas exchange, pulmonary hemodynamic and lung mechanics' properties. In the second phase, we evaluated the mechanical properties of lungs submitted to the same conditions of the first phase. Cold ischemic lungs developed fulminant edema during the first 15 min of ex-vivo reperfusion, whereas gas exchange, hemodynamic and mechanic properties of lungs insufflated to TLC and ventilated during 10 min prior to reperfusion were similar to fresh lungs. After the pulmonary vascular flush pulmonary impedance and alveolar collapsed area increased significantly. The insufflation to TLC and 10 min of tidal ventilation reduced the lung impedance and the percentage of alveolar collapsed area. Lung preservation techniques disarrange alveolar architecture, which lead to ischemia-reperfusion injury; recruitment maneuvers decrease the pulmonary inhomogeneities and protect the lungs against the ischemia-reperfusion injury.

Effects of undernutrition on respiratory mechanics and lung parenchyma remodeling.

Undernutrition thwarts lung structure and function, but there are disagreements about the behavior of lung mechanics in malnourished animals. To clarify this issue, lung and chest wall mechanical properties were subdivided into their resistive, elastic, and viscoelastic properties in nutritionally deprived (ND) rats and correlated with the data gathered from histology (light and electron microscopy and elastic fiber content), and bronchoalveolar lavage fluid analysis (lipid and protein content). Twenty-four Wistar rats were assigned into two groups. In the control (Ctrl) group the animals received food ad libitum. In the ND group, rats received one-third of their usual daily food consumption until they lost 40% of their initial body weight. Lung static elastance, viscoelastic and resistive pressures (normalized by functional residual capacity), and chest wall pressures were higher in the ND group than in the Ctrl group. The ND group exhibited patchy atelectasis, areas of emphysema, interstitial edema, and reduced elastic fiber content. The amount of lipid and protein in bronchoalveolar lavage fluid was significantly reduced in the ND group. Electron microscopy showed 1) type II pneumocytes with a reduction in lamellar body content, multilamellated structures, membrane vesicles, granular debris, and structurally aberrant mitochondria; and 2) diaphragm and intercostals with atrophy, disarrangement of the myofibrils, and deposition of collagen type I fibers. In conclusion, undernutrition led to lung and chest wall mechanical changes that were the result from a balance among the following modifications: 1) distorted structure of diaphragm and intercostals, 2) surfactant content reduction, and 3) decrease in elastic fiber content.