To print: Select File and then Print from your browser's menu

Title: Investigational Model Tests Anti-Exudative Effect Of New Asthma Drugs

URL: http://ajrccm.atsjournals.org/cgi/content/abstract/165/9/1275

American Journal of Respiratory and Critical Care Medicine, 2002; 165: 1275-1279 "Assessment of Microvascular Leakage via Sputum Induction: The Role of Substance P and Neurokinin A in Patients with Asthma"
05/16/2002 11:24:23 AM
By Elda Hauschildt

An investigational model of dual induction microvascular leakage could be useful in testing the anti-exudative effect of newly developed drugs in asthma patients. Dutch researchers from Leiden University Medical Centre describe dual induction as first leakage and then sputum. Testing the model using a potent neurokinin 1 (NK1) agonist in 12 patients with atopic, mild steroid-naïve asthma, the investigators say that microvascular leakage is an important feature in inflammation, but its assessment has seldom been used to monitor airway inflammation in asthma. The researchers evaluated the effects of inhaled substance P, an NK1 agonist and mediator of plasma extravasation, on markers of microvascular leakage in the sputum of the asthma patients. Sputum was in participants before, and 30 minutes after, inhalation of substance P or neurokinin A, the control substance. Markers of leakage in induced sputum included [a₂-macroglobulin, ceruloplasmin, albumin and fibrinogen. Substance P induced a significant increase in levels of a₂-macroglobulin, ceruloplasmin and albumin. Inhaled neurokinin A did not induce significant changes. "Increase in sputum leakage markers was not associated with the cumulative dose of substance P."

http://ajrccm.atsjournals.org/cgi/content/abstract/165/9/1275

Copyright © 2009 P\S\L Consulting Group Inc. All rights reserved. Republication or redistribution of P\S\L content is expressly prohibited without the prior written consent of P\S\L. P\S\L shall not be liable for any errors, omissions or delays in this content or any other content on its sites, newsletters or other publications, nor for any decisions or actions taken in reliance on such content.