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Research Article Free access | 10.1172/JCI105506

Lung Tissue Resistance in Diffuse Interstitial Pulmonary Fibrosis

H. Bachofen and M. Scherrer

Department of Medicine, Inselspital, University of Berne, Berne, Switzerland

†

Address requests for reprints to Dr. H. Bachofen, Dept. of Medicine, Inselspital, University of Berne, 3000 Berne, Switzerland.

*

Submitted for publication June 24, 1966; accepted October 6, 1966.

Supported by the Swiss National Science Foundation and the Science Foundation of the University of Berne.

Find articles by Bachofen, H. in: PubMed | Google Scholar

Department of Medicine, Inselspital, University of Berne, Berne, Switzerland

†

Address requests for reprints to Dr. H. Bachofen, Dept. of Medicine, Inselspital, University of Berne, 3000 Berne, Switzerland.

*

Submitted for publication June 24, 1966; accepted October 6, 1966.

Supported by the Swiss National Science Foundation and the Science Foundation of the University of Berne.

Find articles by Scherrer, M. in: PubMed | Google Scholar

Published January 1, 1967 - More info

Published in Volume 46, Issue 1 on January 1, 1967
J Clin Invest. 1967;46(1):133–140. https://doi.org/10.1172/JCI105506.
© 1967 The American Society for Clinical Investigation
Published January 1, 1967 - Version history
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Abstract

1) Measured during spontaneous breathing in ten patients with diffuse interstitial lung disease, total pulmonary resistance averaged 3.53 ± 1.56 cm H2O per L per second; airway resistance, 1.63 ± 0.79 cm H2O per L per second; and lung tissue resistance, 1.90 ± 0.95 cm H2O per L per second (range, 0.89 to 3.96). The lung tissue resistance was on an average about four times higher in patients with lung fibrosis than in ten healthy persons of the same age. No significant difference in airway resistance was found between healthy subjects and patients.

2) In three patients the lung tissue resistance was measured during spontaneous breathing and during panting. Much higher values were found during spontaneous breathing.

3) In patients with lung fibrosis and also in healthy subjects, there seems to have been an inverse correlation between the vital capacity, or the compliance, on the one hand, and the lung tissue resistance on the other. Nevertheless, in patients with lung fibrosis the lung tissue resistance was more increased than could be attributed to the loss of normally compliant lung tissue only.

4) No correlation was found between the lung tissue resistance and severity of impairment of pulmonary gas exchange; especially no relationship appeared to exist between the lung tissue resistance and the alveolar-end capillary PO2 gradient during hypoxia. This result indicates that the pathological alterations producing a measurable end gradient in hypoxia may be independent of the augmentation of the fibrous framework responsible for the stiffening of the lung.

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