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 Vt 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 20μCi · kg^-1 of [methyl³-H]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.