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Effect of acute ozone induced airway inflammation on human sympathetic nerve traffic: A randomized, placebo controlled, crossover study

 
: Tank, J.; Biller, H.; Heusser, K.; Holz, O.; Diedrich, A.; Framke, T.; Koch, A.; Grosshennig, A.; Koch, W.; Krug, N.; Jordan, J.; Hohlfeld, J.M.

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Fulltext urn:nbn:de:0011-n-1633390 (193 KByte PDF)
MD5 Fingerprint: 00acba0240d40c57c22ff2630fb7bb3a
Created on: 28.6.2011


PLoS one. Online journal 6 (2011), No.4, Art. e18737, 7 pp.
http://www.pubmedcentral.nih.gov/tocrender.fcgi?action=archive&journal=440
ISSN: 1932-6203
English
Journal Article, Electronic Publication
Fraunhofer ITEM ()

Abstract
Background: Ozone concentrations in ambient air are related to cardiopulmonary perturbations in the aging population. Increased central sympathetic nerve activity induced by local airway inflammation may be one possible mechanism.
Methodology/Principal Findings: To elucidate this issue further, we performed a randomized, double-blind, cross-over study, including 14 healthy subjects (3 females, age 22-47 years), who underwent a 3 h exposure with intermittent exercise to either ozone (250 ppb) or clean air. Induced sputum was collected 3 h after exposure. Nineteen to 22 hours after exposure, we recorded ECG, finger blood pressure, brachial blood pressure, respiration, cardiac output, and muscle sympathetic nerve activity (MSNA) at rest, during deep breathing, maximum-inspiratory breath hold, and a Valsalva maneuver. While the ozone exposure induced the expected airway inflammation, as indicated by a significant increase in sputum neutrophils, we did not detect a significant estimated treatment effect adjusted for period on cardiovascular measurements. Resting heart rate (clean air: 59 +/- 62, ozone 60 +/- 62 bpm), blood pressure (clean air: 121 +/- 3/71 +/- 2 mmHg; ozone: 121 +/- 2/71 +/- 2mmHg), cardiac output (clean air: 7.42 +/- 0.29 mmHg; ozone: 7.98 +/- 0.60 l/min), and plasma norepinephrine levels (clean air: 213 +/- 21 pg/ml; ozone: 202 +/- 16 pg/ml), were similar on both study days. No difference of resting MSNA was observed between ozone and air exposure (air: 2362, ozone: 2362 bursts/min). Maximum MSNA obtained at the end of apnea (air: 44 +/- 4, ozone: 48 +/- 4 bursts/min) and during the phase II of the Valsalva maneuver (air: 64 +/- 5, ozone: 57 +/- 6 bursts/min) was similar.
Conclusions/Significance: Our study suggests that acute ozone-induced airway inflammation does not increase resting sympathetic nerve traffic in healthy subjects, an observation that is relevant for environmental health. However, we can not exclude that chronic airway inflammation may contribute to sympathetic activation.

: http://publica.fraunhofer.de/documents/N-163339.html