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Research Article Free access | 10.1172/JCI107375
Institute of Respiratory Physiology, Virginia Mason Research Center, and Firland Hospital, Seattle, Washington 98101
Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98101
Find articles by Martin, C. in: JCI | PubMed | Google Scholar
Institute of Respiratory Physiology, Virginia Mason Research Center, and Firland Hospital, Seattle, Washington 98101
Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98101
Find articles by Sugihara, T. in: JCI | PubMed | Google Scholar
Published August 1, 1973 - More info
The length-tension properties of alveolar wall from normal cats were studied before and after exposure to enzymes naturally found in mammals (elastase, trypsin, collagenase, hyaluronidase). Hyaluronidase effected little change while all the proteolytic enzymes altered the mechanical properties of lung tissue. Collagenase removed the “mechanical stop” and the alveolar walls fractured at low forces. The properties of wall exposed to trypsin resembled those of elastase-treated tissue. Elastase increased the extension necessary to reach a given force and increased the maximum length (Lmax) and resting length (Lo). Maximum extensibility (λmax), the ratio of Lmax to Lo, fell with both elastase and trypsin digestion. A reduction in λmax simulates the changes in alveolar wall properties seen in the lungs of the aged and in those with an irreversible diffuse obstructive pulmonary syndrome (DOPSI). Unlike these states, however, the energy loss in stretching alveolar wall increased with elastolysis. Furthermore, the changes in Lo necessary to effect a change in λmax of alveolar wall comparable to that seen in DOPSI were excessive. The altered tissue properties that occur in man with obstructive pulmonary syndromes could not be produced with these proteolytic enzymes or with hyaluronidase.