1. The cardiac effects of artificial inflation of the lungs were studied during reflexly induced apnoea and bradycardia in anaesthetized dogs.2. Reflex apnoea and bradycardia were induced (a) by stimulation of the larynx with water or by electrical stimulation of afferent fibres in the superior laryngeal nerve, or (b) by combined stimulation of the superior laryngeal nerve and carotid body chemoreceptors.3. During combined stimulation of the laryngeal and carotid body inputs, the activation of respiration normally evoked by chemoreceptor stimulation was inhibited whereas the chemoreceptor cardio-inhibitory reflex was facilitated leading to periods of temporary cardiac arrest.4. In spontaneously breathing animals and in those artificially ventilated, lung inflation invariably caused tachycardia.5. Rhythmic artificial inflation of the lungs during the apnoeic period produced by the laryngeal input or by a combination of the laryngeal and chemoreceptor inputs wholly or partly reversed the bradycardia. This occurred using lung inflation volumes within the range of the normal tidal volume and inflation pressures of less than 12 mmHg; the response was independent of the composition of the gas used for inflating the lungs, and occurred at constant P(a, O2) and P(a, CO2). Lung inflation carried out during a reflexly induced arrest of the heart immediately restarted the heart and was accompanied by an exaggerated sinus arrhythmia.6. Evidence is presented that the observed effects of artificial lung inflation are reflex in origin with the vagus nerves as the main afferent and efferent pathways.7. Electrical stimulation of the central end of the cut pulmonary branches of the thoracic vagosympathetic nerves also caused tachycardia and had the same effects as lung inflation in modifying the reflexly induced bradycardia.8. Some clinical implications of these results are discussed.