SUMMARY1. In anaesthetized cats, in which the carotid arterial bifurcation had been denervated and the spinal cord transacted at the cervical level, reversible bradyeardia mediated by the vagus nerves was elicited by temporary arrest of the cranial circulation. Methoxamine was infused intravenously to maintain peripheral vascular resistance, and artificial ventilation was given to avert systemic asphyxia.2. The bradycardia persisted in cats subjected to one or more of the following acute surgical procedures: left vagotomy, mid-collicular decerebration, decerebellation, bulbar transactions at the acoustic striae and inferior fovea, and destruction of the area postrema and the underlying dorsal vagal nuclei. Ischaemia-induced bradycardia was invariably abolished after bilateral vagotomy or the administration of atropine.3. Bradycardia could not be elicited by electrical stimulation of the dorsal vagal nuclei, but was evoked by stimulation of deep structures in the vicinity of the nucleus ambiguus even after destruction of the dorsal vagal nuclei.4. Simultaneous application of ischaemia and electrical stimulation of the medullary cardio-decelerator locus produced convergent occlusion of the vagal response. The effect of ischaemia was inhibited by stimulation of a neighbouring region in the medial reticular formation. These interactions indicate that an interneuronal link is involved in the mechanism of ischaemia-induced bradycardia. 5. It is concluded that the cardio-decelerator response to ischaemia is initiated upstream to the primary efferent vagal motor neurones and that the cardio-inhibitory fibres do not originate in the dorsal vagal nuclei.