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Experimental studies by Dunn (1) demonstrated that multiple embolism of the pulmonary arterioles and capillaries is followed by a temporary inhibition of respiration succeeded by rapid shallow breathing. Dunn attributed this phenomenon to the stimulation of sensory nerve endings in the lungs. This explanation was favored by the fact that the injection of starch produced no alteration in the respiratory rate when both vagi had been previously sectioned.Attracted to this problem by its bearing upon the occurrence of rapid and shallow respiration in lobar pneumonia, Binger and Moore and their associates (2-6) have carried out a carefully planned series of experiments. Their studies chiefly concern the effects of the embolism of pulmonary arterioles and capillaries produced by the intravenous injection of starch grains under varying conditions. These observations were supplemented by other experimentally induced modifications of the pulmonary circulation. In their conclusion (6) to this instructive series of papers they state: "Since rapid and shallow breathing is not the result of (1) anoxemia, (2) increased pCO, and hydrogen ion concentration of the serum, (3) restriction of pulmonary vascular bed by nearly half, (4) increase in resistance to the flow of blood to and from the lungs, (5) the presence of starch grains in the lungs acting as a local irritant, it must be the result of the secondary pathological changes which occur in the pulmonary parenchyma following embolism. The nature of these changes, congestion and edema has been discussed elsewhere. Whether they operate directly on nerve endings or through their influence on lung volume and tissue elasticity is not certain." In their discussion the authors are inclined toward the hypothesis of direct irritation of the vagal nerve endings, 531 on

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