Document Detail


Effect of pancreatic and leukocyte elastase on hydraulic conductivity in lung interstitial segments.
MedLine Citation:
PMID:  15298987     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
P K Houtz; P D Jones; N E Aronson; L M Richardson; S J Lai-Fook
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2004-08-06
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  97     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-11-08     Completed Date:  2005-04-06     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2139-47     Citation Subset:  IM    
Affiliation:
Center for Biomedical Engineering, University of Kentucky, Lexington, KY 40506-0070, USA.
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MeSH Terms
Descriptor/Qualifier:
Albumins / 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:
HL-36597/HL/NHLBI NIH HHS; HL-40362/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Albumins; EC 3.2.1.35/Hyaluronoglucosaminidase; EC 3.4.21.36/Pancreatic Elastase; EC 3.4.21.37/Leukocyte Elastase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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