The location and excitation of pulmonary deflation receptors by chemical substances

Abstract

1. Deflation fibres from the intact chest of the cat can be identified by observing that inflation of the lungs abolishes the discharge produced by phenyl diguanide and that this discharge reappears when the lungs collapse. 2. Some deflation receptors in the intact chest were stimulated by collapse of the lungs without chemical sensitization. This indicates that in some cats these receptors may be activated normally during rapid expiratory efforts. 3. The injection-discharge time shortened as the dose of phenyl diguanide injected into the right atrium was increased. However, increasing the dose did not influence the intensity of the discharge. 4. The stimulating effect of 5-hydroxytryptamine was not affected by a previous injection of dibenzyline; in this respect deflation receptors differ from smooth muscle. 5. Nicotine and urethane stimulated and sensitized the deflation receptors. The injection-discharge time was shorter than that following phenyl diguanide. Unexpectedly, however, the duration and intensity of the discharge produced by nicotine and urethane were also shorter than those produced by phenyl diguanide. 6. Acetylcholine stimulated and sensitized some deflation receptors. This response was abolished by atropine. The injection-discharge time following acetylcholine was greater than that following phenyl diguanide. In other respects the discharges produced by the two substances were similar. It was concluded that the activation time of acetylcholine for stimulating deflation receptors is the longest, and that of nicotine and urethane the shortest; phenyl diguanide and 5-hydroxytryptamine occupy an intermediate position. 7. Large doses of potassium chloride and veratrum alkaloids did not stimulate the receptors. 8. Discharges in deflation fibres were again shown to produce reflex slowing of the heart. 9. Insufflation of the lungs with ether, trichlorethylene and chloroform stimulated and sensitized the deflation receptors. This was followed by depression or total loss of excitability of the receptors. A varying degree of depressed excitability was also found after all the chemical substances which stimulated the deflation receptors. 10. The results have provided conclusive evidence that the deflation receptors are located in the respiratory bronchioles, atria or the alveoli.