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The breathing of anoxic mixtures causes an increase in the pulmonary arterial pressure of animals (1-4) and man (5-7). This effect has been attributed to a local action of the anoxic mixture on the blood vessel walls resulting in a constriction of the pulmonary arterioles and pre-capillaries and an increase in pulmonary arterial pressure. Vagotomy and stellate ganglionectomy do not change the vascular response to the breathing of anoxic mixtures in the cat (1).The effect of breathing 100% oxygen on the pulmonary arterial pressure has been investigated in animals (1,3,4,8) but not adequately in man. Euler and Liljestrand (1) found that pure oxygen caused a fall in the pulmonary arterial pressure of cats which did not appear to these investigators to be the result of decreased blood flow, but rather to a dilatation of the pulmonary vasculature. The response to oxygen was not affected by vagotomy and stellate ganglionectomy. Ergotamine, yohimbine, and atropine (9) did not alter the decrease of pulmonary arterial pressure which resulted from oxygen breathing. This paper reports observations on the effect of breathing 100% oxygen on the pulmonary arterial pressure of patients with pulmonary tuberculosis and mitral stenosis. METHODSTwo groups of patients were studied. One group consisted of 21 individuals with pulmonary tuberculosis who were studied 27 times. These were all patients with 1Aided by a grant from the Life Insurance MedicalResearch Fund. 2Medical Director of the National Jewish Hospital at Denver.S Public Health Service Postdoctorate Research Fellow of the National Heart Institute.4Fellow of the National Research Council.moderately and far advanced pulmonary tuberculosis (NTA criteria) whose disease was chiefly unilateral. The second group consisted of 17 individuals with rheumatic heart disease manifested by mitral stenosis who were studied 25 times. The morning of the catheterization, the patients received .09 gram of nembutal orally and arrived at the laboratory one hour later in the fasting state. Pulmonary artery catheterization was performed in the usual fashion. A blood sample was taken from the brachial artery for determination of the control oxygen saturation, and pressure-pulse records of the pulmonary arterial pressure were made. When the control pressure level had been established the patient was given 100% oxygen' by BLB mask for a period of four minutes. In 12 instances pulmonary arterial pressure tracings were made continuously during and for ten to 12 minutes after oxygen administration, but in the majority a record was made only when oxygen had been given for three minutes. A sample of brachial arterial blood was withdrawn at the fourth minute of oxygen administration for determination of oxygen saturation.Arterial blood samples were analyzed for oxygen content and capacity by the method of Van Slyke and Neill (10), and more recently by the Scholander-Roughton syringe method (11). The pulmonary arterial pressure was recorded with a Hathaway Blood Pressure Control Unit and Oscillograph ...