Abstract
1. Cats were anaesthetized with a mixture of chloralose and urethane, and were artifically ventilated. 2. An open pneumothorax was provided by two large-bore tubes which were sealed in the sixth intercostal space on each side. They were connected to a Fleisch pneumotachograph. Phasic changes in central inspiratory neuronal activity were measured quantitatively as changes in the volume of the pneumothorax during temporary interruption of artificial respiration, the volume of the lungs being held constant at their end-expiratory level. In this way the activity of slowly adapting pulmonary stretch receptors was maintained constant. 3. Reflex cardioinhibitory responses were elicited by stimulation of (a) the carotid body chemoreceptors by intracarotid injections of cyanide; (b) the arterial baroreflex by controlled elevations of the blood pressure; (c) cardiac receptors by left atrial injections of veratridine; and (d) pulmonary C fibres (including J receptors) by right atrial injections of phenylbiguanide. 4. The effects of central inspiratory neuronal activity on pulse interval were assessed by comparing the values observed during the inspiratory and expiratory phases of the respiratory cycle in the control state and during stimulation of each cardiovascular receptor group. 5. The carotid chemoreceptor-induced bradycardia measured during the expiratory phase of respiration was reduced during inspiration to a value of about 15% of control. The central inspiratory drive was less effective in altering the reflex responses from the arterial baroreceptors and cardiac receptors, the corresponding values being 42 and 51% respectively. 6. In contrast, the bradycardia evoked by pulmonary C fibre stimulation was not significantly affected by the central inspiratory drive. 7. The differential nature of the modulation by the central inspiratory drive occurred independently of the integrity of the sympathetic nerve supply to the heart indicating that the cardiac efferents involved were largely fibres in the vagus nerves. 8. The possible explanation of these results in terms of central mechanisms is discussed.