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Cardiac output measurements during cardiac catheterization were obtained in normal subjects for several grades of treadmill exercise. Femoral venous blood was sampled and the A-V oxygen difference for the exercising leg obtained. Measurements of central and femoral A-V oxygen difference and total oxygen uptake were also obtained in normal subjects during supine rest and during standing. When subjects merely stood, the A-V oxygen difference for the leg increased (whether the leg bore weight or not) much more than did that for the whole body. During treadmill walking femoral A-V oxygen difference was usually no greater than that during standing. Cardiac output was smaller and total body A-V oxygen difference was greater for treadmill walking than for supine bicycle exercise in which comparable levels of oxygen uptake were achieved. It is clear that change in posture alters the cardiac output response to exercise. An important aspect of the altered response was a marked difference in the circulation within the leg for these two postures both at rest and during exercise. Submitted on August 8, 1960

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Each of ten steers taken for 9 weeks to 12,700 ft. (Mt. Evans, Colorado) showed a marked increase in pulmonary artery (PA) pressure. Three animals had PA pressures above 90 mm Hg and one developed right heart failure. The bovine species is remarkable for the severe pulmonary hypertension which develops during chronic hypoxia rather than for an excessive PA pressure response to acute hypoxia. The rate at which the pulmonary hypertension developed at 12,700 ft. was extremely rapid compared to that at 10,000 ft. Therefore, not only the duration of the hypoxic stimulus but also its severity determine the response. The severity of the stimulus was augmented by the absence of a sustained increase in ventilation at high altitude. The pressure rise with acute hypoxia during the control period at low altitude and the dramatic fall in PA pressure when oxygen was administered at high altitude provided evidence for hypoxia-induced pulmonary vasoconstriction as an important mechanism in bovine pulmonary hypertension. Submitted on June 6, 1962

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