Central modulation of arterial chemo‐baroreflex control by propofol during severe arterial hypoxia in the rabbit

Abstract

During hypoxia specific deficits in neural control caused by propofol (2,6‐diisopropylphenol) anesthesia (Prop) are unknown. Dose‐related effects were analysed in rabbits with and without carotid body denervation (CBD) to partition arterial chemo‐baroreflex control. Minute ventilation (VE), tidal volume (VT), respiratory frequency (f), heart rate (HR), mean arterial pressure (MAP) were measured in 12 awake rabbits mask‐breathing room air, then 15 minutes of low oxygen air (PaO2 < 35 mm Hg), during Prop alone (0.2 and 0.5 mg kg−1min−1i.v.), and during matched Prop plus hypoxia. Prop alone caused dose‐related depression in f and rise in HR. Prop plus hypoxia abolished bradycardia, while MAP, VE and VT effects remained intact. CBD eliminated all chemoreflex responses to hypoxia and MAP fell while HR rose, effects enhanced by Prop in a dose‐related way. It is concluded that during Prop, carotid body function for respiratory and MAP defense is functionally intact. Central activation of the vagus is inhibited selectively, because electrical stimulation of peripheral vagus during Prop evokes normal bradycardia blocked by atropine. By contrast, Prop inhibits arterial baroreflex‐vagosympathetic defense against widespread hypoxic vasodilatation. We speculate that the data reflect dominant central GABAA receptor agonist effects on the arterial chemo‐baroreflex arc. Funding: ANZCA and HMRI.