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Variability in preterm lamb lung mechanics after intra-amniotic endotoxin is associated with changes in surfactant pool size and morphometry. Am J Physiol Lung Cell Mol Physiol 287: L992-L998, 2004. First published July 9, 2004; doi: 10.1152/ajplung.00158.2004.--Antenatal exposure to intra-amniotic (IA) endotoxin initiates a complex series of events, including an inflammatory cascade, increased surfactant production and alterations to lung structure. Using the low frequency forced oscillation technique as a sensitive tool for measurement of respiratory impedance, we aimed to determine which factors contributed most to measured changes in lung mechanics. Respiratory impedance data obtained from sedated preterm lambs exposed to either IA injection with saline or 20 mg of endotoxin 1, 2, 4, and 15 days before delivery at 125 days gestation were studied, and association with indexes of standard lung morphometry, inflammatory response, and alveolar surfactant-saturated phosphatidylcholine (Sat PC) pool size was demonstrated. Reduction in tissue impedance with increasing interval between exposure and delivery was evident as early as 4 days after IA endotoxin injection, coinciding with resolution of inflammatory reaction, increased alveolar surfactant pools, and contribution of alveolar ducts to the parenchymal fraction, and a later decrease in the tissue component of the parenchymal fraction. Decreases in tissue damping (resistance) were more marked than decreases in tissue elastance. Log alveolar Sat PC accounted for most variability in tissue damping (88.9%) and tissue elastance (73.4%), whereas tissue fraction contributed 2 and 6.4%, respectively. The alveolar Sat PC pool size was the sole factor contributing to change in tissue hysteresivity. No changes were observed in airway resistance. Despite the complex cascade of events initiated by antenatal endotoxin exposure, variability in lung tissue mechanics is associated primarily with changes in alveolar Sat PC pool and lung morphology. fetal organ maturity; lung compliance; oscillometry; respiratory mechanics

Impact of microvascular circulation on peripheral lung stability. Am J Physiol Lung Cell Mol Physiol 287: L879-L889, 2004. First published June 18, 2004; 10.1152/ajplung.00263.2003.--The involvement of pulmonary circulation in the mechanical properties was studied in isolated rat lungs. Pulmonary input impedance (ZL) was measured at a mean transpulmonary pressure ([Ptp.sub.mean]) of 2 cm[H.sub.2]O before and after physiological perfusion with either blood or albumin. In these lungs and in a group of unperfused lungs, ZL was also measured at [Ptp.sub.mean] values between 1 and 8 cm[H.sub.2]O. Airway resistance ([R.sub.aw]) and parenchymal damping (G) and elastance (H) were estimated from ZL. End-expiratory lung volume (EELV) was measured by immersion before and after blood perfusion. The orientation of the elastin fibers relative to the basal membrane was assessed in additional unperfused and blood-perfused lungs. Pressurization of the pulmonary capillaries significantly decreased H by 31.5 [+ or -] 3.7% and 18.7 [+ or -] 2.7% for blood and albumin, respectively. Perfusion had no effect on [R.sub.aw] but markedly altered the [Ptp.sub.mean] dependences of G and H forced oscillations; alveolar wall; elastin; end-expiratory lung volume

Study of isolated dog lungs reveals that the timing and magnitude of pressure application at the airway entrance is crucial for initiating the avalanche process of alveolar recruitment. Pathological conditions including excessive intrabronchial fluid and reduced pulmonary elasticity may cause changes in this process. A model to describe the process reveals that power-law distributions are similar to that of self-organized critical systems.