The pulmonary consequences of a deep breath

Terence E. Nicholas, John H.T. Power, Heather A. Barr

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    113 Citations (Scopus)


    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.

    Original languageEnglish
    Pages (from-to)315-324
    Number of pages10
    JournalRespiration Physiology
    Issue number3
    Publication statusPublished - Sept 1982


    • Atelectasis
    • Compliance
    • Diffusing capacity
    • Isolated perfused lung
    • Lung distension
    • Peak inspired pressure
    • Rat
    • Sigh
    • Surfactant
    • Yawn


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