Document Detail


Acute stress-induced increases in exhaled nitric oxide in asthma and their association with endogenous cortisol.
MedLine Citation:
PMID:  20709818     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
RATIONALE: psychosocial stress is known to influence the pathophysiology of asthma. Although stress has been linked to serum markers of inflammatory activity and exaggerated response to allergen challenge in asthma, few studies have examined inflammatory activity in the airways linked to psychosocial stress alone. Furthermore, although studies have demonstrated lower levels or reactivity of endogenous cortisol in asthma, the association with airway inflammatory activity in stress remains unexplored.
OBJECTIVES: we therefore studied airway inflammation and cortisol response to a standardized laboratory task inducing acute psychosocial stress.
METHODS: airway inflammation by the fraction of exhaled nitric oxide (FeNO) and saliva cortisol were sampled before and up to 45 minutes after experimental challenge with the Trier Social Stress Test in 20 adult patients with asthma and 19 healthy control subjects. Respiratory inductive plethysmography was used to control for changes in ventilatory activity that impact FeNO levels.
MEASUREMENTS AND MAIN RESULTS: FeNO levels were generally higher in patients with asthma than healthy control subjects and salivary cortisol levels were lower. Increases in cortisol levels were observed after the stress protocol in both groups (P < 0.001). FeNO levels at the time of peak cortisol increase after stress were significantly higher than before stress in both groups (P < 0.05). FeNO increases were independent of changes in ventilation. In patients with asthma, higher cortisol levels and stronger increases in cortisol after stress were significantly associated with smaller increases in FeNO (P < 0.05).
CONCLUSIONS: acute psychosocial stress alone increases airway inflammatory markers and this increase is attenuated by stronger stress-related activity of the hypothalamic-pituitary-adrenal axis in asthma.
Authors:
Thomas Ritz; Erica S Ayala; Ana F Trueba; Charles D Vance; Richard J Auchus
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-13
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  183     ISSN:  1535-4970     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-03     Completed Date:  2011-03-22     Revised Date:  2012-05-29    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  26-30     Citation Subset:  AIM; IM    
Affiliation:
Department of Psychology, Southern Methodist University, P.O. Box 750442, Dallas, TX 75275-0442, USA. tritz@smu.edu
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Asthma / metabolism*,  physiopathology
Breath Tests
Exhalation*
Female
Forced Expiratory Volume
Humans
Hydrocortisone / metabolism*
Male
Middle Aged
Nitric Oxide / analysis*
Radioimmunoassay
Saliva / metabolism*
Severity of Illness Index
Stress, Psychological / metabolism*
Young Adult
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide; 50-23-7/Hydrocortisone

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


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