Description:
Many preterm infants require mechanical ventilation as life-saving therapy.However, ventilation-induced overpressure can result in lung diseases.Considering the lung as a viscoelastic material, positive pressure inside thelung results in increased hydrostatic pressure and tissue compression. Toelucidate the effect of positive pressure on lung tissue mechanics and cellbehavior, we mimic the effect of overpressure by employing an uniaxial loadonto fetal and adult rat lungs with different deformation rates. Additionally,tissue expansion during tidal breathing due to a negative intrathoracic pressurewas addressed by uniaxial tension. We found a hyperelastic deformationbehavior of fetal tissues under compression and tension with a remarkablestrain stiffening. In contrast, adult lungs exhibited a similar response only duringcompression. Young’s moduli were always larger during tension compared tocompression, while only during compression a strong deformation-ratedependency was found. In fact, fetal lung tissue under compression showedclear viscoelastic features even for small strains. Thus, we propose that the fetallung is much more vulnerable during inflation by mechanical ventilationcompared to normal inspiration. Electrophysiological experiments withdifferent hydrostatic pressure gradients acting on primary fetal distal lungepithelial cells revealed that the activity of the epithelial sodium channel(ENaC) and the sodium-potassium pump (Na,K-ATPase) dropped duringpressures of 30 cmH2O. Thus, pressures used during mechanical ventilationmight impair alveolar fluid clearance important for normal lung function.