THE reflex enhancement of respiration observed by Heymans, Bouckaert and Dautrebande [1930] when the blood in the carotid sinus was hypercapnic or anoxeemic, makes it very probable that under such conditions, augmentor impulses pass up to the respiratory centres. Up to the present, however, in Her in g's nerve (whose section abolishes these reflexes) only impulses coming from the stretch receptors of the sinus have been definitely observed [Bronk, 1931; Bronk and Stella, 1932 a, b;Heymans and Rijlant, 1933]. Afferent discharges which could not be ascribed to the action of endosinual pressure and appeared in circumstances in which the augmentor impulses would have been expected, were sometimes noticed. Thus Bronk [1931 (personal communication)], while recording from the intact nerve of the rabbit, occasionally observed a discharge produced as the result of anoxsemia, which persisted after death of the animal, i.e. when the systemic blood-pressure had dropped to zero. Recently Heymans and Rijlant [1933] also described an increased activity in He rin g's nerve during asphyxia of the rabbit, which they were unable to attribute to any difference in the bloodpressure. In neither case was any evidence given which excluded the possibility that these discharges were merely indicative of an irregular activity of the stretch receptors themselves, abnormally excited by the conditions of the blood. This objection is a very serious one, especially in view of the work of Matthews [1933], who found that the stretch end-organs of mammalian muscle discharge spontaneously, often at a very high frequency as the result of occlusion of the circulation. He also observed that such a spontaneous discharge could be obtained in the decerebrate animal by occluding the trachea long enough for convulsions