[Estimation of pulmonary diffusion capacity for oxygen in man at rest, by means of hypoxic rebreathing method].
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The acute dose-dependent effects of nifedipine on the pulmonary diffusing capacity for CO and other lung function indices were investigated in patients with chronic obstructive pulmonary disease (COPD) in a randomized double-blind, cross-over, placebo-controlled trial. Seventeen successive, clinically stable, moderate COPD patients with pulmonary hypertension and 15 control subjects were included in the study. The diffusing capacity of the lungs for carbon monoxide (DLCO) was measured with the single-breath method. Nifedipine (10 and 20 mg) and placebo were administered sublingually at room air. Nifedipine (10 and 20 mg) increased DLCO and DLCO/alveolar volume; however, a larger effect was observed with 10 mg. In addition, nifedipine increased the pulmonary capillary blood volume dose-dependently while arterial oxygenation was improved only with 10 mg nifedipine. Venous shunt was significantly increased with 20 mg nifedipine whereas spirometric parameters were unaffected. The percent DLCO change with 10 or 20 mg nifedipine was inversely correlated with baseline DLCO, but not with the severity of obstruction. Nifedipine did not have any effect in the control group, except for mild hypotension and a reflex increase in the heart rate. It is concluded that 10 mg nifedipine probably has an effect on the pulmonary circulation in moderate COPD patients with pulmonary hypertension.
Pulmonary tissue volume (Vti), carbon monoxide diffusing capacity, membrane diffusing capacity, pulmonary capillary blood flow and pulmonary capillary blood volume were measured in ninety (54 men and 36 women) healthy lifetime nonsmokers using an inert gas rebreathing technique. Prediction equations were generated using multiple linear regressions with height and age as the independent variables. Normalizing the data by dividing by functional residual capacity eliminated all sex differences. In contrast to the other variables, normalized pulmonary tissue volume did not correlate with any of the independent variables tested. Therefore, an average normalized Vti value can be recommended as a reference value
Pulmonary function studies were done in 21 soldiers (low landers) posted at high altitude (average height 4773 metres) for prolonged periods (average 77.09 months), who had developed excessive polycythaemia, mean haemoglobin concentration being 23.06 g/dl. Studies revealed significant reduction in diffusion capacity of lungs which gradually returned to normal on sojourn at low altitudes for 70 days. Both the degree of polycythaemia and reduction in lung diffusion capacity were much more pronounced in smokers than in non-smokers. Vital capacity did not show any difference in these subjects while forced expiratory volume in 1 sec and ratio of forced expiratory volume to vital capacity (FEV1/VC) revealed only obstructive features in smokers.
To clarify the mechanism of the disturbance of alveolar gas exchange in idiopathic pulmonary fibrosis, various pulmonary function tests were performed on 7 patients with the disease, of which 5 were defined histo-pathologically and 2 clinically. On 4 of all patients, detailed comparative studies of histopathological findings to pulmonary functions were carried out additionally. As the results, marked decreases of total lung capacity, pulmonary diffusing capacity (DLco) and Pao2 were observed. On exercise, the improvement of DLco or physiologic dead space (VD/VT) was hardly seen, while AaDO2 increased markedly. Ventilation (VA), perfusion (Q), and VA/Q ratio examined by 133Xe scintigram distributed more evenly over the entire lung fields than controls. These may suggest that the disturbance of alveolar gas exchange is mainly due to the elongation of the distance for diffusion in the membrane.
Healthy children evidence smaller values of cardiorespiratory function than adults, but these are in proportion to the smaller body size. At birth, the distribution of muscle fibres and the activity of enzymes in muscle are different from in adults, but these differences disappear at about age 6. On the other hand, muscle fibre thickness increases from birth to about 18 years of age and this is concurrent with increases in muscular strength. The increase in maximal oxygen consumption (VO2max) that accompanies growth and maturation in the human has been attributed in the main to appreciating muscle mass. During exercise, heart rate and cardiac output increase in the child as in the adult, but the heart rate in the child is greater and the stroke volume smaller. Furthermore, the arteriovenous difference in oxygen is greater in the exercising child than in the adult. Children also evidence a diminished blood pressure response to exercise. It seems that control of ventilation at exercise is the same in children as in adults, but exercise ventilation has been reported to be less efficient in the child. The young are less capable of regulating core temperature at exercise than adults and are more readily dehydrated. Very limited data suggest that muscle energy substrate storage and utilisation in children are such that they are less capable of anaerobic metabolism than adults. Generally, children respond to aerobic training as do adults, but such training in the first decade of life has been reported to have negligible effects. Blood lipid levels in children seem to be favourably influenced by persistent endurance activity. Ventilatory efficiency of children at exercise is augmented by aerobic training. Maximal values of ventilation and breathing frequency are increased in children and youth by endurance training. Conflicting data exist regarding the influence of training upon the child's vital capacity. Pulmonary diffusion capacity in well trained children has been seen to be greater than in untrained youngsters and many workers have reported increased VO2max as an outcome of endurance training. Limited data indicate that the nature of training may alter muscle fibre distribution in youthful athletes, and that muscle fibre hypertrophy can be induced in the young by means of strength and power training.(ABSTRACT TRUNCATED AT 400 WORDS)
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The results of 64 membranes diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) estimations were analysed to assess the clinical significance of these measurements. These estimations were performed on 18 healthy subjects, 19 patients with mitral valvular involvement of rheumatic aetiology, 15 patients with chronic bronchitis and emphysema, 8 patients with chronic bronchitis alone, and 4 patients with pulmonary embolism. It was observed that Dm correlated very well with the pulmonary diffusing capacity (DLCO) measured during the inhalation of room air in all the groups of subjects. In patients with rheumatic heart disease, the DLCO was affected little by even large changes in Vc, whereas it ran closely parallel to the Dm in these subjects. In the past Dm has been considered to be an unreliable estimation, varying greatly as a result of small errors in the measurement of DLCO. This appears to be relatively true only in normal subjects having low Vc/Dm ratio. In a majority of diverse clinical conditions where the Vc/Dm ratio is increased, the Dm becomes a more reliable estimation. In these patients the DLCO itself is a good index of the membrane diffusing capacity.
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Pulmonary membrane diffusing capacity (Dm) and pulmonary capillary blood volume (Vc) measurements were carried out in 21 patients with untreated tropical eosinophilia and 21 healthy controls matched for age, sex, height, and smoking habit. The mean single breath transfer factor (Dco) and the mean membrane diffusing capacity were significantly lower (p less than 0.001) in patients with tropical eosinophilia compared with control subjects. However, the mean capillary blood volume was not significantly different (p greater than 0.2). The positive correlations between Dm and transfer factor (r = 0.825), between Dm and effective alveolar volume (VA) (r = 0.721), and between Dco and VA (r = 0.774) were also highly significant (p less than 0.001) in study patients prior to treatment. These data suggest that reduction in single breath transfer factor in untreated tropical eosinophilia may be due to a reduction in membrane diffusing capacity, which in turn may be due to a reduction in area of membrane available for diffusion, as evidenced by the significantly reduced VA (p less than 0.001) in these patients. Since pulmonary capillary blood volume was normal, the pulmonary perfusion was within normal limits. Following three weeks of treatment with diethylcarbamazine citrate, although there was a significant rise in single breath transfer factor (p less than 0.001) and membrane diffusing capacity (p less than 0.05), both Dco (p less than 0.01) and Dm (p less than 0.01) continued to be significantly lower than those of control subjects. However, pulmonary capillary blood volume did not show any change (p greater than 0.2).
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