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The Effects of Remifentanil on the Cardiorespiratory Responses to Severe Arterial Hypoxia in the Rabbit
Author(s) -
Quail Anthony Walker,
Cottee David Bruce,
Johnstone Janice Maree,
White Saxon William
Publication year - 2016
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.30.1_supplement.758.2
Subject(s) - remifentanil , anesthesia , medicine , bradycardia , heart rate , tidal volume , respiratory rate , arterial blood , hypoxia (environmental) , ventilation (architecture) , reflex bradycardia , blood pressure , respiratory system , chemistry , propofol , oxygen , mechanical engineering , organic chemistry , engineering
We have previously shown that the central vagus is sensitive to several modern anesthetics (Quail et al 2013, 2015). Remifentanil is an ultra‐short acting synthetic opiate widely used in anesthesia, sedation, obstetrics and analgesia. Opiates can act at the carotid body (McQueen and Ribeiro 1980; Mayer, et al., 1989) and at the commissural nucleus of the solitary tract in the CNS (Zhang et al. 2011), but effects on the integrated components of chemoreflex control are unknown. We examined the hypothesis that components of the cardiorespiratory responses evoked by severe arterial hypoxia (PaO2 < 35 mm Hg) are selectively altered by remifentanil. Six female NZ White rabbits were cannulated via an ear artery and vein (lidocaine 1%). Minute ventilation (VE), tidal volume (VT), respiratory frequency (f), heart rate (HR), mean arterial pressure (MAP) and oxygen saturation (ear SpO2) were measured in conscious rabbits breathing room air, followed by 5 minutes of hypoxia (FiO2 7–8%). After one hour recovery, rabbits breathed room air during i.v. remifentanil (0.1, 0.2, 0.3, or 0.4 mcg/kg/min), followed by matched hypoxia, then recovery breathing room air. Two doses of remifentanil were studied on each of two days, one week apart. Arterial blood samples were taken for blood gas analysis. Data were analysed using repeated measures ANOVA. In rabbits breathing room air remifentanil caused a dose‐related fall in f, VE and HR (P<0.01), while VT and MAP were unchanged. During remifentanil and hypoxia, the reflex bradycardia evoked in conscious rabbits was largely preserved (P<0.05) in a dose‐related manner. The increase in VT remained intact, however the increase in VE was attenuated, with f increasing from a lowered baseline. Remifentanil produced dose‐dependent sedation. We conclude that vagal control of heart rate with remifentanil during severe hypoxia is maintained, while the effects on VE, VT and f appear selective. The data suggest the actions of remifentanil on cardiorespiratory control during hypoxia are mainly central, rather than at the carotid body. Support or Funding Information John Hunter Charitable Research Trust and Hunter Medical Research Institute