B E V E G~, S., A. HOLMGREN and B. JONSSON. The eJect of body position on the circulation at rest and during exercise, with special reference to the inzuence on the stroke volume. Acta physiol. scand. 1960. 49. 279-298.-In 10 healthy, adult, male subjects the hemodynamics have been studied by the aid of heart catheterization at rest and during work both in supine and sitting positions. The cardiac output was on the average 2.2 l/min less in the sitting than in the supine position, both at rest and during exercise. In the supine position, the stroke volume was constant at rest and during exercise. I n the sitting position, the stroke volume at rest was 40 per cent smaller than in the supine. I t increased considerably with mild work, but not significantly with a n even heavier work load. It never reached the values obtained in the supine position, even during heavy work. The arterio-venous oxygen difference was larger in the sitting than in the supine position, both at rest and during work. During heavy work, the oxygen transport per heart beat was the same in the supine and the sitting positions, and the physical working capacity (work performed per heart beat) was also of the same order.

Eight well trained athletes (cyclists) with large dimensions of the circulatory system were studied with heart catheterization at rest and during exercise at 800 and 1,600 kpm/min both while sitting and supine. The results are compared with data from non‐athletes. The cardiac output at rest and during work showed the same relation to the oxygen uptake as in nonathletes. The cardiac output was less in the sitting than in the supine position by 2.6 1/min at rest and 1.8 1/min during heavy work, due to a smaller stroke volume in the sitting position in both groups. On transition from rest to exercise the stroke volume increased 9 % in the supine and 48 % in the sitting position. After these initial changes the stroke volume remained constant during continued exercise with the heavier load in both body positions. The difference in stroke volume between supine and sitting position averaged 43 ml at rest and 9 ml during heavy exercise. The stroke volume during work in the supine position showed the same relation to the blood volume as in the nonathletes. The stroke volume was larger than expected from the size of the heart, when compared with the previously demonstrated relationship in nonathletes. The rate of work, performed at pulse rate 170, bore approximately the same relationship to the stroke volume during exercise in both groups. The larger oxygen transport capacity of these athletes as compared to nonathletes is explained by a larger stroke volume. During exercise the ventricular filling pressures were higher than in nonathletes.

Right heart catheterization has been performed in 18 healthy subjects, 14 males and 4 females, including estimation of cardio‐vascular pressures and cardiac output at rest and during different intensities of exercise in recumbent position. During exercise the cardiac output increased linearly with the oxygen uptake. The increase of the arterio‐venous oxygen difference in relation to the work load or the pulse rate was higher in the males than in the females. With change from rest to work the stroke volume increased slightly but significantly in the males. By increasing work load it successively decreased to the size at rest. There was a high correlation between the stroke volume on one hand and the work performed at pulse rate 170, the heart volume, and the blood volume on the other. The mean pressure in the pulmonary artery was 5 mm Hg higher during exercise than at rest but was constant at different work loads. The end‐diastolic pressure in the right ventricle and the mean pulmonary venous pressure (PC V‐pressure) did not change significantly with the increase in pulse rate.

Palmitate-9, 10-H3 has been infused intravenously at a constant rate together with various C14-labeled fatty acids in healthy subjects at rest and during exercise. No significant differences in the rates of fractional turnover were found between H3-labeled palmitate and C14-labeled palmitate or oleate. Retention of a considerably larger fraction of C14-labeled linoleate in the blood plasma precluded accurate assessment of its fractional turnover rate. The rates of oxidation of palmitate-I-C14, palmitate-U-C14, oleate-I-C14, and linoleate-I-C14 during exercise were similar. The relative abundance of palmitate, oleate, and linoleate in the free fatty acids of plasma changed little during exercise. It is concluded that palmitate-I-C14 is a valid tracer for measuring the turnover rate and oxidation of at least three-fourths of circulating free fatty acids under the conditions of study. Recycling of radioactivity in triglyceride fatty acids of plasma was similar for H3-labeled palmitate and C14-labeled palmitate and oleate, both at rest and during exercise. The plasma concentration of glycerol increased promptly with exercise. Changes in its concentration closely followed those in the turnover rate of free fatty acids, but were of greater magnitude. plasma glycerol during exercise; plasma triglycerides, formation from different FFA; respiratory quotient during exercise Submitted on October 4, 1963

SummaryThe influence on airway conductance of inhaled aerosols of prostaglandin F2c (PGF2oc), histamine, and prostaglandin E2 (PGE2) was studied in 10 patients with spirometrically reversible bronchial asthma and in 10 healthy subjects with no history of lung disorder. Both groups responded with bronchoconstriction after inhalation of PGF,oc but the asthmatic patients were about 8,000 times more sensitive to the compound than were the healthy controls. In the patients, but not in the controls, PGF2x often caused a long-standing decrease in airway conductance with symptoms resembling allergen-provoked asthmatic attacks. On the other hand, the patients showed less than a 10-fold increase in sensitivity to histamine, and the ratio of histamine: PGF2,x doses causing a 50%o decrease of airway conductance was 2 6:1 and 2,400:1 in controls and patients respectively. Inhalation of PGE2 while moderately but consistently increasing airway conductance in controls, had a variable -occasionally slight bronchoconstrictive-effect in patients. The decrease in airway conductance by a given dose of PGFcc was little modified by the simultaneous inhalation ofa 100-times higher PGE, dose. It is suggested that endogenous, locally formed PGF2La may play an important part in the pathogenesis of bronchial asthma.