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Interstitial fibrosis and collateral ventilation.

D M Berzon, H Menkes, A M Dannenberg

    Journal of Applied Physiology (Bethesda, Md. : 1985)
    |July 1, 1986
    PubMed
    Summary
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    Interstitial fibrosis increases collateral resistance (Rcoll) by reducing lung volume or damaging airways. Pulmonary interdependence does not compensate for these fibrotic changes.

    Area of Science:

    • Pulmonary Physiology
    • Respiratory Medicine
    • Pathology

    Background:

    • Interstitial fibrosis can alter collateral flow resistance (Rcoll) through complex mechanisms.
    • Potential effects include increased Rcoll due to decreased lung volume or destroyed collateral channels.
    • Alternatively, emphysematous changes near fibrosis might decrease Rcoll.

    Purpose of the Study:

    • To investigate the impact of interstitial fibrosis on collateral airflow resistance.
    • To determine if pulmonary interdependence influences Rcoll in fibrotic lung regions.

    Main Methods:

    • Measurements of Rcoll were taken at functional residual capacity (FRC) in nine dogs.
    • Bleomycin was instilled locally into lung segments to induce fibrosis.
    • Rcoll was also assessed at a higher lung volume (12 cmH2O above FRC).

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    Main Results:

    • Interstitial fibrosis led to increased Rcoll in treated lung segments.
    • Lung inflation caused a similar proportional decrease in Rcoll in both fibrotic and non-fibrotic regions.
    • No compensatory increase in collateral pathways was observed.

    Conclusions:

    • Increased Rcoll in fibrotic lung segments is attributed to decreased lung volume or direct fibrotic involvement of collateral pathways.
    • Pulmonary interdependence does not disproportionately increase fibrotic region volume or decrease Rcoll during inflation.