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Central/Peripheral Chemoreceptor Interaction in the Unanesthetized Dog: Evidence for Hyperaddition
Author(s) -
Blain Gregory,
Smith Curtis,
Henderson Kathleen,
Dempsey Jerome
Publication year - 2010
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.24.1_supplement.799.4
Subject(s) - hypercapnia , chemoreceptor , normocapnia , central chemoreceptors , carotid body , hypoxic ventilatory response , anesthesia , perfusion , central nervous system , stimulation , pco2 , medicine , endocrinology , respiratory system , acidosis , receptor
We assessed the contribution of carotid body chemoreceptors (CB) to the ventilatory response to specific CNS hypercapnia in the unanesthetized awake dog. We used extracorporeal blood perfusion of the reversibly isolated carotid sinus to maintain normal blood gases (normoxic, normocapnic perfusate) at the CB, to inhibit the CB (hyperoxic, hypocapnic perfusate), or to stimulate the CB (hypoxic, normocapnic perfusate) while the systemic circulation, and therefore the central nervous system (CNS), was exposed to normocapnia and 4 progressive levels of hypercapnia for 7 minutes at each level. Relative to control (normoxic and normocapnic perfusion), we found that CB inhibition decreased the slope of the ventilatory response to CNS hypercapnia in all dogs by 80% on average (N=6) whereas CB stimulation increased the slope of the ventilatory response to CNS hypercapnia in all dogs by 123% on average (N=4). We conclude that the gain of the CNS CO 2 /H + chemoreceptors is critically dependent on CB afferent activity and the CNS/CB interaction results in hyperadditive ventilatory responses. Supported by NIH/NHLBI & American Heart Association.