The effects of positive end-expiratory pressure (PEEP) on lung tissue resistance (Rti) and dynamic elastance (Edyn,L) were examined separately during histamine-induced lung constriction and after saline lung lavage in anesthetized paralyzed New Zealand White rabbits. During mechanical ventilation in the open-chest state, Rti and Edyn,L were estimated by fitting the appropriate signals to the equation of motion of the single-compartment linear model of the lung. Data were analyzed in relation to the structural damping hypothesis, which assumes that energy dissipation (Rti) and energy storage (Edyn,L) within the lung tissues are coupled at a fundamental level; the coupling parameter, termed hysteresivity (eta), = Rti.omega/Edyn,L, where omega is angular frequency. Under baseline conditions, elevation in PEEP resulted in significant increases in both Rti and Edyn,L, with eta remaining unchanged. During induced constriction and after lung lavage, Rti and Edyn,L significantly increased relative to their baseline values. During histamine-induced constriction, increasing PEEP was associated with increases in Edyn,L, whereas Rti and eta were reduced. After lung lavage, elevation in PEEP from 5 to 7 cmH(2)O was associated with proportional increases in Rti and Edyn,L, resulting in a relative constancy of eta. By contrast, when PEEP was decreased from 5 to 3 cmH(2)O, the values of Rti increased, whereas Edyn,L remained unchanged, resulting in significant increases in eta. Collectively, these findings suggest that the effects of PEEP on Rti during agonist-induced constriction and after perturbations of the gas-liquid interface are dependent on the state of alveolar/airway stability.