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Although it has been recognized for some time that anoxia may result in an elevation of the pres- sure in the pulmonary artery, the mechanism of this response has not been satisfactorily explained.Von Euler and Liljestrand (1) in 1946 demon- strated in anesthetized cats that breathing 10%o to 11 %7o oxygen in nitrogen caused a rise in pulmonary artery pressure which was not affected by vagotomy or excision of the stellate ganglia, and which they therefore attributed to a direct effect of anoxia on the pulmonary vessels.Although left atrial pressure was sometimes recorded directly (2), no measurements of cardiac output were made, so that the pressor effects of changes in vascular resistance could not be separated conclusively from those due to variations in blood flow.Motley and his associates (3) in 1947 demon- strated the pulmonary hypertensive effect of anoxia in five unanesthetized human subjects, using the technique of cardiac catheterization.A slight fall in cardiac output occurred simultaneously with the rise in pulmonary arterial pressure and an in- verse relationship between the two was suggested.Nevertheless, the two possible mechanisms of (a) stasis in the smaller pulmonary vessels associ- ated with a decreased output of the left ventricle, or (b) pulmonary arteriolar constriction, could not be segregated except by inference.Recent reviews (4-6) of the pulmonary circula- tion in general, have accepted the role of anoxia in the pathogenesis of pulmonary hypertension, and have implied that the mechanism involved is pulmonary vasoconstriction.However, vasoconstric-
Westcott et al. (Sat,) studied this question.