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Contribution of carotid body chemoreceptors to the eupneic drive to breathe in the intact awake canine
Author(s) -
Blain Gregory M,
Smith Curtis A,
Henderson Kathleen S,
Demspey Jerome A
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.957.3
Subject(s) - chemoreceptor , carotid body , anesthesia , perfusion , central chemoreceptors , ventilation (architecture) , chemistry , tonic (physiology) , control of respiration , respiratory system , peripheral chemoreceptors , medicine , electrophysiology , receptor , physics , thermodynamics
We used extracorporeal perfusion of the reversibly isolated carotid sinus to determine the effects of specific carotid body (CB) chemoreceptor inhibition on eupneic ventilation (VI) in the resting, awake, unanesthetized, intact dog. 4 female dogs were studied when CB was perfused with 1) normoxic and normocapnic blood, and 2) hyperoxic (> 500 mmHg) and hypocapnic (20 mmHg) blood to maximally inhibit the CB tonic activity. We found that perfusion per se (normoxic ‐ normocapnic) had no effect on V I . In contrast, CB inhibition caused an immediate and substantial reduction in V I which reached a nadir (‐56%) within 29 sec and a steady state (‐24%) within 100 sec. At steady state, this V T ‐induced (‐17%) hypoventilation persisted throughout continued CB perfusion (up to 25 min) despite a marked CO 2 retention (+9 mmHg) and respiratory acidosis (pH a = 7.27). Consistent with hypoventilation, mean electrical activity of diaphragm EMG was also reduced (‐24%) during CB inhibition. Ventilation returned toward control values within ∼27 sec when exogenous CB perfusion was terminated. We interpret these data to mean that CB chemoreceptor contributes as much as one‐half or more to the total drive to eupnea in the normoxic, intact, awake animal, and that this contribution consists of both a tonic sensory input to respiratory controller as well as a strong modulatory effect on the central chemoreceptor responsiveness to CO 2 . NHLBI/NIH ‐ AHA