| Effect of pancreatic and leukocyte elastase on hydraulic conductivity in lung interstitial segments. | |
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MedLine Citation:
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PMID: 15298987 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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 cmH(2)0, and mean interstitial pressure was either 0 or 10 cmH(2)O. Elastase caused an increase in flow in approximately 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. |
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Authors:
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P K Houtz; P D Jones; N E Aronson; L M Richardson; S J Lai-Fook |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S. Date: 2004-08-06 |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 97 ISSN: 8750-7587 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2004 Dec |
Date Detail:
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Created Date: 2004-11-08 Completed Date: 2005-04-06 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 2139-47 Citation Subset: IM |
Affiliation:
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Center for Biomedical Engineering, University of Kentucky, Lexington, KY 40506-0070, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Albumins
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pharmacokinetics Animals Capillary Permeability / physiology Extravascular Lung Water / metabolism* Hyaluronoglucosaminidase / metabolism Leukocyte Elastase / metabolism* Lymph / metabolism Models, Biological Pancreatic Elastase / metabolism* Pulmonary Alveoli / blood supply, enzymology* Pulmonary Circulation / physiology Rabbits |
| Grant Support | |
ID/Acronym/Agency:
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HL-36597/HL/NHLBI NIH HHS; HL-40362/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Albumins; EC 3.2.1.35/Hyaluronoglucosaminidase; EC 3.4.21.36/Pancreatic Elastase; EC 3.4.21.37/Leukocyte Elastase |
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