Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of these receptors to phenyl diguanide, potato starch, 5-hydroxytryptamine and nicotine, and their rôle in respiratory and cardiovascular reflexes

Abstract

1. The endings of certain vagal afferent fibres have been located in the lungs, using the method of locating visceral receptors described recently [Paintal, 1954 a). These receptors were sensitized specifically by pulmonary deflation. 2. The fibres were found to be normally inactive. With the cats' chest intact it was sometimes possible to evoke a rapidly adapting discharge of impulses by suction of air from the trachea or by collapse of the lungs with open chest. The receptors were unaffected by anoxia but they could be sensitized by congestion of the lungs. 3. The action potentials of these fibres were the smallest yet observed in vagal afferent fibres; in most deflation fibres the potentials barely exceeded the base-line noise level. It is estimated that the conduction velocities of the majority of the fibres are below 6 m./sec. 4. The receptors were stimulated by injection of phenyl diguanide, starch, nicotine and 5-hydroxytryptamine. Some of the receptors yielded considerably reduced responses following subsequent injections of phenyl diguanide, but the majority of them were little affected. 5. The injection-discharge time following rapid injections of phenyl diguanide into the right atrium of cats with intact chest ranged from 0·9 to 2·7 sec. With open chests the injection-discharge time could be varied by injecting the drug during different phases of artificial respiration; the values were increased when the drug was injected during inflation of the lungs. The drug sensitized the receptors from 7 to 21 sec. 6. Apart from the usual response of respiratory inhibition, phenyl diguanide on many occasions gave rise to respiratory acceleration without the initial period of apnœa. This response could be elicited more frequently by small doses of phenyl diguanide, but it could also be produced by large doses injected slowly. 7. Nicotine, starch and HT gave rise to early reflex respiratory and cardiac responses identical with those following phenyl diguanide. 8. It is suggested that the deflation receptors are primarily responsible for producing reflex respiratory acceleration (rapid shallow breathing) and that they cause respiratory inhibition when greatly stimulated by drugs. They may also take part in the reflex bradycardia following injections of the drugs used in this investigation. 9. The receptors are not connected with the bronchial circulation or with any part of the broncho-pulmonary shunt, but with the pulmonary circulation. They are probably situated near the alveoli. 10. In many cats the deflation fibres were encountered grouped in bundles. At present the only way of isolating them is by injecting drugs which stimulate them. 11. These deflation receptors are quite different from the so-called deflation receptors described previously [Adrian, 1933; Paintal, 1953 b].