BJURSTEDT, H., C. M. HESSER, G. LILJESTRAND and G. MATELL. Effects of posture on alveolar-arterial CO, and 0, differences and on alveolar dead space in man. Acta physiol. scand. 1962. 54. 65-82. -The increase in ventilation and lowering of the end-tidal Pco, after changing from the supine to the standing position were observed to be associated with a significant rise in the arterial to end-tidal CO, tension difference (average + 2.1 mm Hg) in addition to an increased effective alveolar to arterial 0, tension difference (+ 4.8 mm Hg). All dead spaces increased, the alveolar dead space (= the physiological minus the anatomical dead space) on an average by 28 ml. Assuming an unchanged distribution of ventilation this can be expressed as corresponding to 6 per cent of the alveoli being unperfused. A lowering of the alveolar Pco2 during standing is thus in part due to an increased arterial to end-tidal GO, tension difference. The end result is also influenced by a certain metabolic acidosis (average decrease in BHCO,B, 7 0.6 mM/l), in addition to peripheral retention of CO,. The Eff. VA/VE ratio decreased in all subjects, indicating a decline in the respiratory gas exchange efficiency by an average of 6 per cent. The changes observed may be explained as a consequence of the influence of gravityon the blood flow and its distribution not only in the systemic but also in the pulmonary circulation. Already in 1914 LILJESTRAND a n d WOLLIN showed that the alveolar CO, tension in m a n is lower during motionless standing than in the supine position. These authors had also confirmed a n d extended the old observation that assuming the up-right position calls forth a n increase in the pulmonary ventilation (cf. LILJESTRAND and WOLLIN 1913). Both the lowered alveolar 5-623015. Acta physiol. scand. Vol. 54. 65 66 H. BJURSTEDT ET A L .C:O, tension and the increase in pulmonary ventilation have been confirmed in numerous investigations (d. The mechanisms underlying the fall in the alveolar (20, and the increase in pulmonary ventilation after changing from the supine to the standing position are not fully understood. T h e former effect cannot be explained xilelj-b y an increased blowing off of CO, b y the hyperventilation, since the amount of C 0 2 eliminated during several minutes of motionless standing does not exceed the 0, uptake, as demonstrated b y HITCHCOCK and FER-GUSON as well as by RAHS and AXENT. These authors referred the lowered alveolar Pc:p2 during standing to impaired CO, elimination from the lungs, caused by the decrease in cardiac output with a concomitant CO, retention in the tissues and in venous blood, especially in the lo\ver portion of the body.By using special tecliniqucs for the continuous and simultaneous recording of blood gas changes 011 the centrifuge, rather drastic changes in the pulmonary circulation and gas exchange have been observed, both in the dog ;BARK, BJVRSTEDT and COLERIDGE 1959) and in man (BARR 1961 a). I n the espcriments to be reported beloiv, using similar techniques on the tilt-tabl...