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Hypoxic ventilatory depression is attenuated by blockade of K(ATP) channels and adenosine receptors in the isolated bullfrog brainstem
Author(s) -
Hedrick Michael S.,
Chen Anna K.
Publication year - 2009
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.23.1_supplement.621.24
Subject(s) - bullfrog , adenosine , medicine , respiratory system , hypoxia (environmental) , endocrinology , hypoxic ventilatory response , adenosine receptor , chemoreceptor , biology , receptor , brainstem , chemistry , anesthesia , oxygen , agonist , organic chemistry
This study examined the role of K(ATP) channels and adenosine receptors in regulating the hypoxic ventilatory response in isolated brainstems of post‐metamorphic bullfrogs ( Lithobates catesbeiana ). We used an in vitro brainstem preparation from post‐metamorphic frogs (N=12; T‐K stages >25) that was superfused with oxygenated artificial CSF (20‐22 ºC) and generated spontaneous respiratory motor output measured by suction electrodes attached to cranial nerves (CN) V, X and XII. Control brainstems superfused with hypoxic artificial cerebrospinal fluid (aCSF) bubbled with 98% N 2 /2% CO 2 produced a ventilatory depression marked by significant reductions in lung burst frequency within 15‐30 min that were sustained for 3 h of hypoxia. Reoxygenation with 98% O 2 /2% CO 2 returned lung burst frequency to control levels. Hypoxic brainstems superfused with aCSF containing the K(ATP) channel blocker, 2,3‐butanedione monoxime (BDM;500 μM) and the adenosine receptor antagonist, theophylline (100 μM), did not exhibit a hypoxic ventilatory depression until 90 min after the onset of hypoxia, but returned to control levels upon reoxygenation. These data suggest that the hypoxic ventilatory depression observed in the isolated bullfrog brainstem is mediated in part by K(ATP) channels and/or adenosine receptors. Supported by NIH SO6 GM48135.