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Arachidonic acid stimulates avian intrapulmonary chemoreceptor (IPC) discharge
Author(s) -
Petelle Kristin M.,
Migdalene Jaime A.,
Hempleman Steven C.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.721.7
Subject(s) - noxious stimulus , chemistry , arachidonic acid , chemoreceptor , inhalation , pentobarbital , anesthesia , stimulus (psychology) , medicine , endocrinology , nociception , biochemistry , receptor , enzyme , psychology , psychotherapist
Bronchial inflammation initiated by noxious agents or disease can affect the rate and depth of breathing by activating pulmonary afferents in mammals. To investigate this in birds, the inflammatory intermediate arachidonic acid (AA) was injected intravenously into pentobarbital‐anesthetized, ventilated ducks ( Anas platyrhynchos, n=11 ) and cycle‐triggered stimulus histograms of IPC action potential discharge to CO 2 stimulus steps were recorded. IPC discharge with 2 mg/kg AA was unchanged from vehicle control, but 8 and 20 mg/kg AA significantly stimulated mean IPC discharge and reduced phasic adaptation (ANOVA, p<0.05). AA effects were not altered by pretreatment with indomethacin (5 mg/kg, n=3). Interpretation: if inhaled noxious agents liberate AA in bird lungs, IPC discharge could be increased, which would decrease V T and increase f R , limiting further inhalation exposure. Support: NIH R15 HL087269 ‐02.