Sökning: WFRF:(Sjodin B.)
> (2015-2019) >
Urinary excretion o...
-
Bood, JRKarolinska Institutet
(författare)
Urinary excretion of lipid mediators in response to repeated eucapnic voluntary hyperpnea in asthmatic subjects
- Artikel/kapitelEngelska2015
Förlag, utgivningsår, omfång ...
-
American Physiological Society,2015
Nummerbeteckningar
-
LIBRIS-ID:oai:prod.swepub.kib.ki.se:131743906
-
http://kipublications.ki.se/Default.aspx?queryparsed=id:131743906URI
-
https://doi.org/10.1152/japplphysiol.00301.2015DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
Exercise-induced bronchoconstriction displays refractoriness manifested as a decreased response to repeated exercise challenge within hours. The refractoriness may be attenuated by inhibition of the biosynthesis of prostaglandins (PG). The aim of the study was to determine which PGs and other lipid mediators are excreted during the refractory period. First, 16 subjects with mild stable asthma performed two repeated 4-min challenges with eucapnic voluntary hyperpnea (EVH) 1 and 3 h apart. There was a similar degree of refractoriness in both protocols (∼15% protection). The 1-h interval was too short to study mediator excretion because the urinary levels did not return to baseline before the second challenge. With the 3-h protocol, there was increased urinary excretion of cysteinyl-leukotrienes and metabolites of the mast cell product PGD2after both challenges. Next, another eight subjects performed two 6-min challenges with EVH 3 h apart, which produced a greater bronchoconstrictor response than the 4-min protocol (30.0 ± 5.4 vs. 17.7 ± 1.5%; P = 0.0029) and a greater degree of refractoriness (∼30%). Analysis by ultra-performance liquid chromatography triple quadrupole mass spectrometry confirmed excretion of the bronchoconstrictor cysteinyl-leukotrienes and PGD2during both challenges. In addition, there was increased excretion of the bronchoprotective PGE2, and also of the main metabolite of PGI2. This is the first report of excretion of PGE2and PGI2during the refractory period to EVH challenge, suggesting that they may mediate the refractoriness. Maintained excretion of PGD2and leukotriene E4following the repeat challenge argues against mast cell mediator depletion as the mechanism of refractoriness.
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Sundblad, BMKarolinska Institutet
(författare)
-
Delin, IKarolinska Institutet
(författare)
-
Sjodin, MKarolinska Institutet
(författare)
-
Larsson, KKarolinska Institutet
(författare)
-
Anderson, SD
(författare)
-
Wheelock, CEKarolinska Institutet
(författare)
-
Dahlen, SEKarolinska Institutet
(författare)
-
Dahlen, BKarolinska Institutet
(författare)
-
Karolinska Institutet
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Journal of applied physiology (Bethesda, Md. : 1985): American Physiological Society119:3, s. 272-2791522-16018750-7587
Internetlänk
Hitta via bibliotek
Till lärosätets databas