Mephentermine increased maximum breathing capacity in emphysema patients due to partial relief of existing bronehospasm. Small variations occurred in tidal volume, arterial-blood saturation, O
2
uptake and CO
2
removal per liter ventilation, and in respiratory quotient. There was an increase in expiratory minute volume, alveolar ventilation, frequency of respiration, O
2
consumption, CO
2
elimination, and arterial-blood pH; a decrease occurred in physiological dead space, physiological dead space/tidal volume ratio, and CO
2
content and tension in arterial blood. These changes were marked in normal individuals and in mitral stenosis patients, in contrast to the minimal effects obtained in emphysema cases. Bronehodilatation in emphysema, reduction of the physiological dead space and physiological dead space/tidal volume ratio, and changes in both direction in arterial-blood saturation as well as circulatory effects suggest that mephentermine affects the ventilation-perfusion relationships throughout the lung. The disproportionate increase in expiratory minute volume and frequency of respiration, while arterial-blood findings showed a significant decrease in CO
2
tension and a significant increase in pH, suggests an important central effect. In normal and in mitral stenosis patients, mephentermine produced an increase in heart rate, a decrease in mean right-atrial pressure, and an increase in cardiac output as a result of myocardial stimulation. Changes in pulmonary-artery pressure were variable. Pulmonary arteriolar resistance decreased in all three normal controls and in the majority of mitral stenosis cases, while wedge pressure changed very slightly. These changes are interpreted as pulmonary vaso-dilatation. Systemic pressure increased, while total systemic resistance decreased or remained essentially unchanged. Arteriovenous O
2
difference decreased in most eases with increased cardiac output, and vice versa. Increased cardiac output, associated with unchanged or falling systemic resistances and decreased arteriovenous O
2
difference, suggests vasodilatation with, increased peripheral blood flow. The fact that systemic resistance increases slightly in some cases must mean that vasocon-striction with decreased peripheral blood flow occurred in other vascular areas as a probable compensatory reaction. These effects led to an increase in arteriovenous O
2
difference and a reduction in cardiac output.
