1. Embolism of pulmonary arterioles and capillaries produced by the intravenous injection of starch grains results in a dilatation of the pulmonary artery and the right chambers of the heart. This has been demonstrated both by x-ray studies and direct inspection.

2. The dilatation of the pulmonary artery and heart occurs synchronously with the acceleration of respirations.

3. Dilatation of these structures produced by other means, such as obstruction to the flow of blood to and from the lungs, by gradually clamping either the pulmonary artery (cat and dog) or pulmonary veins (cat) does not, however, give rise to rapid and shallow breathing.

4. The effect of these maneuvers on respiration does not become apparent until respirations suddenly cease.

5. Neither does sudden restriction of the pulmonary vascular bed by clamping the left branch of the pulmonary artery give rise to rapid and shallow breathing, though this procedure may cause an increase in CO2 tension and in hydrogen ion concentration of the blood.

6. Since rapid and shallow breathing is not the result of (1) anoxemia, (2) increased pCO2 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.

7. 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.

8. Various important clinical analogies have been emphasized.

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