In the normocapnic range, middle cerebral artery mean velocity (MCA Vmean) changes approximately 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO2) and a decrease in PaCO2 will reduce the cerebral blood flow by vasoconstriction (the CO2 reactivity of the brain). When standing up MCA Vmean and the end-tidal carbon-dioxide tension (PETCO2) decrease, suggesting that PaCO2 contributes to the reduction in MCA Vmean. In a fixed body position, PETCO2 tracks changes in the PaCO2 but when assuming the upright position, cardiac output (Q) decreases and its distribution over the lung changes, while ventilation (VE) increases suggesting that PETCO2 decreases more than PaCO2. This study evaluated whether the postural reduction in PaCO2 accounts for the postural decline in MCA Vmean). From the supine to the upright position, VE, Q, PETCO2, PaCO2, MCA Vmean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO2Hb) were followed in seven subjects. When standing up, MCA Vmean (from 65.3+/-3.8 to 54.6+/-3.3 cm s(-1) ; mean +/- SEM; P<0.05) and cO2Hb (-7.2+/-2.2 micromol l(-1) ; P<0.05) decreased. At the same time, the VE/Q ratio increased 49+/-14% (P<0.05) with the postural reduction in PETCO2 overestimating the decline in PaCO2 (-4.8+/-0.9 mmHg vs. -3.0+/-1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA Vmean seems to be explained by the reduction in PETCO2 but the small decrease in PaCO2 makes it unlikely that the postural decrease in MCA Vmean can be accounted for by the cerebral CO2 reactivity alone.

In patients with stable asthma, we assayed plasma proteins in the bronchoalveolar lavage fluid to obtain information on plasma exudation into the airways. Fourteen nonsmoking patients with asthma who were in a stable period of their disease and eight nonsmoking healthy volunteers were studied. The ratios of the concentrations of albumin, ceruloplasmin (CP), and alpha-2-macroglobulin (A2M) between blood and epithelial lining fluid were calculated (cQalb, cQCP, and cQA2M). The cQalb was increased in the patients (Mann-Whitney U test, p less than 0.05). In 10 patients the bronchial hyperreactivity was assessed with histamine provocation tests. Significant relationships between the cQalb, cQCP, and cQA2M on the one hand and PC15 on the other hand were found (Spearman's rank correlation: r = -0.62, p less than 0.05; r = -0.61, p less than 0.05; r = -0.79, p less than 0.01, respectively). Fourteen patients were treated with two inhalations of 200 micrograms glucocorticosteroids per day in a 3-month prospective study. Three of them were excluded from further study because of an intercurrent exacerbation of asthmatic symptoms during therapy. In the 11 patients with stable asthma, the cQalb and cQA2M decreased after treatment with inhaled steroids (Wilcoxon's matched pairs signed rank test, p less than 0.03). Our results show that in patients with stable asthma, there is an increased plasma exudation into the airways, most likely caused by an increased respiratory membrane permeability. The plasma exudation correlated with the bronchial hyperreactivity to histamine, and it decreased after corticosteroid therapy.

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Lung function and respiratory symptoms were studied in 40 children aged 8-18 years who had been ventilated for hyaline membrane disease after birth; 11 had had bronchopulmonary dysplasia.Also studied were 38 age matched children who had had hyaline membrane disease but had not required ventilation, 25

Perinatal exposure to Dutch background dioxin levels is rather high. Studies of calamities have shown that dioxins negatively influence the respiratory system. It was hypothesized that perinatal exposure to background dioxin levels leads to lung suboptimality, probably through developmental interference. This study aimed to assess lung function in relation to perinatal dioxin exposure. Spirometry was performed in 41 healthy children (aged 7‐12 y, mean 8.2 y) with known perinatal dioxin exposure. The ratio of forced expiratory volume in 1 s to forced vital capacity (FEV1/FVC ratio) was determined. A complete medical history was taken. The prenatal exposure ranged from 8.74 to 88.8 (mean 34.6) ng TEQ dioxin kg fat−1, measured in breast milk. The postnatal exposure ranged from 4.34 to 384.51 (mean 75.4) ng TEQ dioxin. Twelve children had to be excluded. A significant decrease in lung function in relation to both prenatal (p= 0.045) and postnatal (p= 0.0002) dioxin exposure was seen in the 29 non‐excluded children. A clinical association between chest congestion and perinatal dioxin exposure was seen. Conclusion: Perinatal background dioxin exposure may be inversely associated with the FEV1/FVC ratio.

In order to assess the usefulness of sputum analysis in studying plasma-protein exudation and local secretion of proteins in the airways, we measured specific proteins in the sputum sol phase (SSP) and sputum gel phase (SGP) from patients with stable asthma or chronic obstructive pulmonary disease (COPD). Protein levels in SSP showed relatively small variations between two subsequent visits of each patient (n = 22), as also reflected by intraclass correlation coefficients above 0.79. Protein levels differed between SSP and SGP, but inclusion of the SGP data did not affect the variation of protein levels in sputum. The degree of plasma-protein leakage was estimated from the relative coefficients of excretion (RCE) of alpha 2-macroglobulin and albumin (QA2M/QALB), and of alpha 2-macroglobulin and ceruloplasmin (QA2M/QCP), which do not depend on variable dilution of sputum. Despite the heterogeneity of the study group of 26 patients with asthma (atopic [13] smokers [13], including five patients using inhaled steroids), QA2M/QALB and QA2M/QCP correlated both with bronchial hyperreactivity (Spearman rank: r = -0.45 and r = -0.36, p < 0.05) and with blood eosinophil counts (r = 0.37 and 0.56, p < 0.05). We conclude that protein levels in SSP are relatively constant in patients with stable asthma or COPD; in patients with asthma, the plasma-protein leakage, as measured with the RCE in SSP, appears to correlate with indirect indices of airway inflammation.