Role of pulmonary surfactant in airway closure: a computational study.

A numerical model that simulates airway closure by liquid bridging during expiration has been developed. The effects of both surfactant and time-varying geometry have been included; the model determines the liquid layer flow resulting from a surface tension (Rayleigh) instability, and the computation traces the film's development to closure, yielding pressure, velocity, surface shape, and surfactant concentration distributions. It is found that surfactant is effective in retarding or eliminating liquid bridging through the reduction of the mean surface tension and the action of surface tension gradients. The former effect is also critical in minimizing the magnitude of the negative pressure in the liquid layer and thus presumably in reducing the tendency for airway compliant collapse.

Dynamic surface tension of surfactant TA: experiments and theory.

A bubble surfactometer was used to measure the surface tension of an aqueous suspension of surfactant TA as a function of bubble area over a range of cycling rates and surfactant bulk concentrations. Results of the surface tension-interfacial area loops exhibited a rich variety of phenomena, the character of which varied systematically with frequency and bulk concentration. A model was developed to interpret and explain these data and for use in describing the dynamics of surface layers under more general circumstances. Surfactant was modeled as a single component with surface tension taken to depend on only the interfacial surfactant concentration. Two distinct mechanisms were considered for the exchange of surfactant between the bulk phase and interface. The first is described by a simple kinetic relationship for adsorption and desorption that pertains only when the interfacial concentration is below its maximum equilibrium value. The second mechanism is "squeeze-out" by which surfactant molecules are expelled from an interface compressed past a maximum packing state. The model provided good agreement with experimental measurements for cycling rates from 1 to 100 cycles/min and for bulk concentrations between 0.0073 and 7.3 mg/ml.

Airway closure and reopening assessed by the alveolar capsule oscillation technique.

An alveolar capsule oscillation technique was used to determine 1) the lobe pressure and volume at which airways close and reopen, 2) the effect of expiration rate on closing volume and pressure, 3) the phase in the breathing cycle at which airway closure occurs, and 4) the site of airway closure. Experiments were conducted in excised dog lobes; closure was detected by an abrupt increase in the input impedance of surfacemounted alveolar capsules. Mean transpulmonary pressure (Ptp) at closure was slightly less than zero (Ptp = -2.3 cmH2O); the corresponding mean reopening pressure was Ptp = 14 cmH2O. The expiration rate varied between 1 and 20% of total lobe capacity per second and had no consistent effect on the closing volume and pressure. When lung volume was cycled up to frequencies of 0.2 Hz, closure generally occurred on expiration rather than inspiration. These observations support the conclusion that mechanical collapse, rather than meniscus formation, is the most likely mechanism producing airway closure in normal excised dog lungs. Analysis of measured acoustic impedances and reopening pressures suggests that closure occurs in the most peripheral airways. Reopening during inspiration was often observed to consist of a series of stepwise decreases in capsule impedance, indicating a sequence of opening events.