Role of surface tension and tissue in rat lung stress relaxation.

Abstract When the volume of the lung is maintained constant after an initial change of volume, stress relaxation (SR) occurs as a slow decay of transpulmonary pressure (P TP ). In order to define which structure in the lung is responsible for SR a multiple exponential fitting of the P TP variation has been made. Exercised rat lungs were placed in a fluid-filled box with trachea connected to atmosphere and submitted to stepwise changes of volume. Single volume steps (0.2 ml) were performed for lungs filled with either air or saline and the variations of P TP were monitored until steady state was reached. An exponential model (time constant = 6.5 ± 0.4 (SD) and 92 ± 6 s) described adequately the SR for air-filled lungs (n = 6) whereas only one exponential ( time constant = 6.7 ± 1.3 s) was required for saline-filled lungs. Multiple volume step experiments were also performed in air-filled lungs to obtain pressure volume loops. These hysteresis loops have been adequately simulated by use of the exponential model. It can be concluded that (1) lung tissue and air-liquid interface are both responsible for the SR, with, respectively, short and long time constants and (2) the same relaxation function is able to describe both stress relaxation and static hysteresis in such experimental conditions.