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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 97/6/2139    most recent 00567.2004v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Houtz, P. K. Articles by Lai-Fook, S. J. Search for Related Content PubMed PubMed Citation Articles by Houtz, P. K. Articles by Lai-Fook, S. J.

Effect of pancreatic and leukocyte elastase on hydraulic conductivity in lung interstitial segments

Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky 40506-0070

Submitted 3 June 2004 ; accepted in final form 27 July 2004

Elastase-induced changes in flow were used to quantify the degradation of lung interstitial elastin. Degassed rabbit lungs were inflated with silicon rubber via airways and vessels. The lungs were cut into 1-cm-thick sections. Two chambers were bonded to each section to enclose the interstitium surrounding an arterial segment. Flow of albumin solution (0–5 g/dl) between the chambers was followed by that of the albumin solution with 0.25 g/dl pancreatic elastase solution. Driving pressure was 5 cmH₂0, and mean interstitial pressure was either 0 or 10 cmH₂O. Elastase caused an increase in flow in 70% of the interstitial segments and a reduction in flow in the remaining segments. The elastase-induced response in flow was independent of both albumin concentration and mean interstitial pressure. Leukocyte elastase (5 units/dl) produced flow responses similar to those of 0.25 g/dl pancreatic elastase. The increased flow of leukocyte elastase was reduced by a subsequent flow with 0.25 g/dl pancreatic elastase but enhanced by a subsequent flow with a 10-fold lower concentration. A change in the order of the elastase flows reversed the concentration-dependent responses. This behavior suggests a complex interaction among the interstitial fibers after degradation by pancreatic and leukocyte elastase. Endogenous elastase-induced increases in interstitial permeability might affect blood-lymph barrier permeability, whereas elastase-induced cessation of flow might be related to the alveolar septal wall destruction observed in emphysema.

reflection coefficient; rabbit; lung fluid balance; hyaluronidase; emphysema