The effects of artificial lung inflation on reflexly induced bradycardia associated with apnoea in the dog

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Abstract
The cardiac effects of artificial inflation of the lungs were studied during reflexly induced apnea and bradycardia in anesthetized dogs. Reflex apnea and bradycardia were induced by stimulation of the larynx with water, by electrical stimulation of afferent fibers in the superior laryngeal nerve or by combined stimulation of the superior laryngeal nerve and carotid body chemoreceptors. During combined stimulation of the laryngeal and carotid body inputs, the activation of respiration normally evoked by chemoreceptor stimulation was inhibited; the chemoreceptor cardio-inhibitory reflex was facilitated leading to periods of temporary cardiac arrest. In spontaneously breathing animals and those artificially ventilated, lung inflation caused tachycardia. Rhythmic artificial inflation of the lungs during the apneic 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 12mmHg. The response was independent of the composition of the gas used for inflating the lungs, and occurred at constant Pa,O2 [arterial partial pressure of O2] and Pa,CO2 [arterial partial pressure of 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. Evidence is presented that the effects of artificial lung inflation are reflex in origin and the vagus nerves act as the main afferent and efferent pathways. 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.