H. Ghezzo

Lack of acute effects of ascorbic acid on spirometry and airway responsiveness to histamine in subjects with asthma

Sixteen adult subjects with asthma in a clinical steady state were studied. On day 1, after baseline spirometry, they underwent four histamine inhalation tests with functional recovery between each test. The provocative concentration causing a 20% fall in FEV1 (PC20) was obtained after each test. On days 2, 3, and 4, after baseline spirometry, active and placebo ascorbic acid (2 gm) was administered orally, double-blind, according to a 4.3.1 two-treatment crossover study design. One hour later, spirometry was performed, and PC20 was reassessed. We found no significant changes in FEV1 and FVC after ascorbic acid as compared with placebo administration. There was no difference between PC20 on days 2, 3, and 4 and by standardizing for the four PC20 results obtained on day 1. We conclude that ascorbic acid has no acute bronchodilator effect and does not alter bronchial responsiveness to histamine in subjects with asthma.

Inhaled lignocaine does not alter bronchial hyperresponsiveness to hyperventilation of dry cold air in asthmatic subjects

It has been hypothesized that bronchoconstriction due to exercise and hyperventilation is caused by the stimulation of irritant receptors in the upper airways. However, controversial results have been reported on the effect of lignocaine, which can inhibit the stimulation of these receptors. The aim of this study was to investigate the effect of inhaled lignocaine on bronchial responsiveness to hyperventilation of cold dry air in asthmatic subjects. Eight adult asthmatic subjects in a clinical steady state came on four different days (two placebo and two active days in random order) with a maximum interval of 3 weeks. After assessment of forced expiratory flow rates, inhalation of either phosphate‐buffered saline (placebo) or lignocaine solution (40 mg) was carried out in a single‐blind fashion. The technician was not aware which medication was being inhaled, but the asthmatic subject knew which drug it was by the sensation in his or her throat. Forced expiratory flow rates were reassessed 15 min after the nebulization; then, the subjects were asked to inhale cold dry air (−20°C) in progressively increasing levels of ventilation (7.5, 15, 30 and 60 1/min and maximum voluntary ventilation). PD20 was interpolated from the dose‐response curve, relating the dose of cold air on a noncumulative logarithmic scale on the abscissa and the percentage change in FEV1 on the ordinate. There were no significant changes in FEV1 and PD20 after inhalation of lignocaine as compared to the placebo. We conclude that inhaled lignocaine does not significantly alter bronchial hyperresponsiveness to hyperventilation of cold air in asthmatic subjects. It is therefore unlikely that receptors in the upper airways could modulate this type of bronchoconstriction.

Distinct temporal patterns of immediate asthmatic reactions due to high- and low-molecular-weight agents

Exposure to occupational agents can cause immediate asthmatic reactions.