1. Pulmonary arterial hypertension was demonstrated in a series of rats that had been kept for 24–31 days in an environment of compressed air, having a barometric pressure of 3040 mm. Hg. The partial pressure of oxygen was 635 mm. Hg, which is equivalent to an 83.6 per cent oxygen mixture at normal barometric pressure.
2. Sclerosing changes in the pulmonary arterioles have been observed which precede the development of demonstrable hypertension in the pulmonary circulation. These vessels showed histological changes that were indicative of injury after 3 days of exposure. There was a thickening of the walls which stained more intensely with eosin, as well as marked perivascular edema and often a narrowing of the lumina. Progressive thickening, narrowing, and hyalinization of the pulmonary arterioles occurred later, after the disappearance of perivascular edema. These changes appeared very similar to the renal arterial lesions seen at autopsy in patients dying from malignant hypertension.
3. Pathological examination did not reveal significant or constant changes from normal in any organs except the lungs and heart. The blood vessels of the systemic circulation showed no pathological change.
4. The walls of the large pulmonary arteries increased in thickness rapidly after the 3rd day of exposure. This change was due to the progressive formation and condensation of fibrous tissue outside of the media and to a lesser extent to thickening of the alternate layers of elastic tissue and smooth muscle in the arterial wall.
5. Marked dilatation of the right ventricle and conus arteriosus as well as small areas of scar tissue formation in the right ventricle were present on prolonged exposure. A few hearts showed larger areas of fibrosis that were visible on macroscopic examination.
6. The systemic arterial blood pressure of a small series of rats exposed to compressed air for 38 days and examined 7 to 10 days after decompression was in each instance less than one-half the average normal pressure.
7. The findings in this study are consistent with the clinical and pathological signs of pulmonary hypertension in man.
8. The anatomical alterations observed in the alveolar units of the lungs were essentially the same as those previously described (1).
9. A method has been devised whereby pulmonary arterial hypertension, accompanied by important sclerotic changes in the arteries of the pulmonary circulation can be induced for investigation.