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. 1989 Oct;417:323–341. doi: 10.1113/jphysiol.1989.sp017804

Differential modulation by pulmonary stretch afferents of some reflex cardioinhibitory responses in the cat.

M B Daly 1, E Kirkman 1
PMCID: PMC1189269  PMID: 2621597

Abstract

1. Cats were anaesthetized with a mixture of chloralose and urethane, and were artificially ventilated, the thorax being opened via a medial sternotomy. 2. Various cardiovascular receptors were stimulated during reflex inhibition of the central inspiratory neurones produced by electrical stimulation of both superior laryngeal nerves simultaneously, while the afferent input from the lungs was held constant by temporarily interrupting artificial respiration, the lungs being held static in their expiratory position. 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) the carotid sinus baroreceptors by raising the pressure in isolated perfused carotid sinus preparations; (d) cardiac receptors by left atrial injections of veratridine, and (e) pulmonary C fibres (including J receptors) by right atrial injections of phenyl biguanide. 4. The effects of single inflations of the lungs on these reflex cardioinhibitory responses were studied and compared with the effects of the various inputs alone. 5. Stepwise increases in lung volume, while having no consistent effect on arterial blood pressure, progressively diminished the arterial chemoreceptor-induced bradycardia to a value of about 7% of the control response without lung inflation. The pulmonary afferents were less effective on reflex responses from other inputs, the corresponding values being: arterial baroreflex, 66%; carotid baroreceptors, 66%, and cardiac receptors, 70%. These effects of lung inflation were abolished by selective denervation of the lungs. 6. In contrast, the size of the bradycardia evoked by pulmonary C fibre stimulation was, on average, unaffected by inflation of the lungs. In some tests the response was actually increased. 7. The differential modulation by lung inflation of these reflex cardioinhibitory responses were the same after upper thoracic sympathectomy indicating that pulmonary afferents and cardiac efferents involved fibres in the vagus nerves. 8. The possible central mechanisms responsible for the differential modulation by lung inflation of cardioinhibitory reflexes are discussed.

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Selected References

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