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Effects of sub‐anesthetic sevoflurane on cardiorespiratory responses to severe arterial hypoxia in the rabbit (709.4)
Author(s) -
O'Donnell Jonathan,
Quail Anthony,
Cottee David,
White Saxon
Publication year - 2014
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.28.1_supplement.709.4
Subject(s) - hypoxia (environmental) , tidal volume , bradycardia , anesthetic , cardiorespiratory fitness , anesthesia , carotid body , chemistry , heart rate , sevoflurane , chemoreceptor , medicine , respiratory system , ventilation (architecture) , endocrinology , peripheral chemoreceptors , blood pressure , oxygen , carotid arteries , mechanical engineering , receptor , engineering , organic chemistry
Volatile anesthetics may alter reflexes to hypoxia through actions at the carotid body chemoreceptors. The effects of sevoflurane (Sev) in sub‐anesthetic concentrations on integrated chemoreflex control during hypoxia are unknown. The cardiorespiratory responses to end‐tidal Sev (0.18%, 0.37% or 1.86%) were studied in 7 rabbits. Ventilation (V E ), tidal volume (V T ), respiratory rate (f), heart rate (HR) and arterial pressure (AP) were measured in awake rabbits breathing room air, then 5 minutes of hypoxia (PaO 2 < 35 mm Hg), during Sev alone, and Sev plus hypoxia. In awake rabbits hypoxia produced an increase in V E and V T ( p <0.05) while f was unchanged. HR fell and AP rose ( p <0.05). During normoxia, V T increased and f decreased with all concentrations of Sev, while V E only fell at 0.37% and 1.86% ( p <0.05). HR increased with at all concentrations while AP decreased at 0.37% and 1.86% ( p <0.05). With hypoxia and Sev, the increase in V T was the same as awake levels at all concentrations associated with a small rise in f ( p <0.05). V E increased to levels seen in the awake state at lower concentrations of Sev but was attenuated at 1.86% ( p <0.05). The hypoxia induced bradycardia and rise in AP were attenuated by increasing doses of Sev and abolished at 1.86% ( p <0.05). Sub‐anesthetic depressant effects of Sev on the cardiorespiratory responses to hypoxia are selective and therefore unlikely to be the result of carotid body inhibition. Grant Funding Source : Supported by John Hunter Hospital Charitable Trust