Asbestos-induced visceral pleural fibrosis reduces pulmonary compliance.

To determine the nature of respiratory functional impairment caused by asbestos-induced visceral pleural fibrosis (VPF) and to discover which pulmonary physiological variable best reveals it, we examined 59 asbestos-exposed construction workers having asbestos-related changes on chest radiographs. Computed tomography scans of the thorax were also performed. Visceral pleural fibrosis was diagnosed in 29 subjects: seven had only VPF, 17 had VPF and pleural plaques, and five had VPF, plaques, and asbestosis. In subjects without VPF, 23 had plaques, six had plaques and asbestosis, and one had only minor fibrotic parenchymal changes insufficient for a diagnosis of asbestosis. Flow-volume spirometry, body plethysmography, static and dynamic compliance, and pulmonary diffusing capacity for carbon monoxide were measured. The subjects with VPF had significantly lower static (p = 0.005) and dynamic (p = 0.007) compliance values than those without. Other respiratory function variables failed to show any significant differences. We conclude that the measurement of static and dynamic compliance is a useful method in assessing pulmonary function impairment caused by visceral pleural fibrosis.

Inhaled budesonide fails to inhibit the PAF-induced increase in plasma leukotriene B4 in man.

1. We studied the ability of inhaled budesonide to modulate PAF-induced acute effects in nine healthy nonsmoking volunteers. Responses in inflammatory cells and mediators in peripheral blood as well as in pulmonary function and circulation were monitored. 2. Inhalation of increasing doses of PAF (total cumulative dose of 500 micrograms) caused a rapid and profound decrease in circulating white blood cells, especially in granulocytes (P less than 0.01), which was turned to an increased number of these cells (P less than 0.05, P less than 0.025, respectively) in the blood samples taken 8 min after completion of the PAF challenge. No changes in the circulating platelets or their thromboxane production were found. Plasma concentrations of histamine or methylhistamine remained unchanged during PAF-inhalation, while plasma LTB4 tripled from the baseline level at 10 min (P less than 0.0005) and was returned to the pre-PAF value at 60 min. 3. PAF inhalation induced a bronchial obstruction (P less than 0.025), but no bronchial hyperresponsiveness to methacholine was found in any of our subjects when measured 24 h after the PAF challenge. Furthermore, PAF caused a decrease in systolic blood pressure (P less than 0.05). 4. Budesonide pretreatment of 400 micrograms twice daily during the preceding 5 days had no effect on any PAF-induced events measured in our study. That fact may also contradict the role of bronchial resident or alveolar cells as a source of the PAF-induced LTB4 burst in plasma. 5. We conclude that in healthy volunteers inhaled PAF induces a marked increase in plasma LTB4, which is not inhibited by inhaled budesonide.(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet-activating factor impairs mucociliary transport and increases plasma leukotriene B4 in man.

We assessed the effect of inhaled platelet-activating factor (PAF) on tracheobronchial clearance, pulmonary function and blood pressure in seven healthy volunteers. After inhalation of 500 micrograms of PAF, retention of radioaerosol in ciliated airways measured at 4 h was 80% higher than in the control recording, and the clearance was reduced by 33% (p less than 0.005). Acetylsalicylic acid (ASA) did not abolish the phenomenon. PAF also decreased forced expiratory volume in one second (FEV1) by 16% (p less than 0.01), which was markedly attenuated by acetylsalicylic acid. The decrease in blood pressure after PAF (p less than 0.01) was not influenced by acetylsalicylic acid. Plasma leukotriene B4 (LTB4) was increased at 20 min after PAF inhalation (without and with ASA: mean 240 and 299 pg.ml.1, respectively) as compared to the baseline (144 and 166 pg.ml.1) and the values at 60 min after the challenge (133 and 178 pg.ml.1; p less than 0.05 and p less than 0.01, respectively). Only three out of seven subjects showed a bronchial hyperresponsiveness to methacholine measured 24 h after PAF. The PAF-induced reduction of mucociliary transport seems to be independent of cyclo-oxygenase products of arachidonic acid metabolism. These autacoids are, however, believed to contribute to the acute bronchial obstruction after PAF inhalation. In addition, inhaled PAF causes a transient increase in plasma LTB4.