The pulmonary consequences of a deep breath

We used the isolated rat lung perfused with Krebs bicarbonate and 4.5% albumin, to examine the effect of a transient increase in peak inspired pressure (PIP). The lung was ventilated with 5% CO2 in O2 at a Vr of 2.5 ml, an f of 60 min-1 and an end expired pressure of 2 cm H2O. After 30 min we increased the PIP from 9 to 18 cm H2O for one breath; following a further 30 sec of normal ventilation we lavaged the lung. The large breath increased the amount of alveolar surfactant phospholipids (PLalv) (control: 7.0 +/- 0.73 (11); large breath: 8.3 +/- 1.33 (14), mean +/- SD in mg . g dry lung-1), and decreased the percentage of PLalv associated with tubular myelin (control: 30.2 +/- 3.49% (9); deep breath: 25.4 +/- 2.99% (9). In rats that had received 20 microCi . kg-1 of [methyl-3H]choline chloride 3 h previously, there was also an increase in the tritium in PLalv expressed as a percent of that in tissue (control: 4.4 +/- 0.77% (5); deep breath: 5.7 +/- 1.0% (7). The deep breath also resulted in an increase in oxygen diffusing capacity. We conclude, that a single deep breath results in the opening of atelectatic alveoli, the release of pulmonary surfactant and possibly also the transfer of PLalv from the tubular myelin to the monomolecular phase.