N emboli were produced in the blood of anesthetized dogs by rapid decompression from air compressed to 65 1b. gauge pressure for 105 min. The condition thus produced was similar to that of acute compressed-air illness. The characteristic symptoms observed were rapid breathing, temporary rise followed by a fall in blood pressure, a retarded pulse rate, O unsaturation of the arterial blood and a marked increase in the arterial-venous difference. The rapid breathing and O unsaturation of the arterial blood are attributed to embolic blockage of the pulmonary circulation. The fall in blood pressure and increased arterial-venous difference is attributed to embolic injury to the nerve tissue which controls circulation. In order to dissipate the emboli the dogs were recompressed to 30 lb. gauge pressure. During this time some of the dogs breathed air and other pure O, to test the efficacy of O therapy in the treatment of compressed-air illness. When the pressure again returned to normal it was observed that when O was breathed, the O unsaturation of the arterial blood was relieved, the respiratory rate returned to a normal value and only a few bubbles remained at autopsy; when air was breathed during recom-pression, a return to normal pressure caused the reformation of bubbles as observed at autopsy, and a return of the rapid breathing and O unsaturation of the arterial blood. The exptl. results justify the use of O to accelerate the absorption of N emboli.