Nitric oxide (NO) appears to play an important role in regulating several biologic functions in the lung, including modulation of pulmonary arterial and bronchial smooth muscle tone. Recent studies have shown that relatively high concentrations of inhaled NO reduce the bronchoconstrictor effect of methacholine in animal models. This raises the possibility that NO inhalation might have therapeutic potential as an alternative bronchodilator. Although investigation of this potential in adults with airway reactivity or bronchial asthma has been reported, data are lacking on the role of NO in the pediatric asthma population. We therefore performed spirometry on 12 children with asthma (mean age 11.1 yrs) at baseline (B), immediately after inhaling 40 ppm NO (NO-1), 10 min after inhaling NO (NO-10), and after inhalation of a standard beta 2-agonist, albuterol (A). Baseline pulmonary functions (% predicted +/- SEM) were FVC of 103.2 +/- 5.6, FEV1 of 82.2 +/- 3.3, FEF-max of 97.0 +/- 3.6, and FEF25-75% of 53.5 +/- 3.3. There were no statistically significant differences between baseline and NO-1 or NO-10 between any of the four pulmonary function parameters measured. Inhaled albuterol, however, resulted in significant improvement (% predicted +/- SEM) in FVC to 109.8 +/- 3.5, FEV1 to 99.7 +/- 2.9, FEFmax to 106.5 +/- 5.1, and FEF25-75% to 84.4 +/- 6.4 compared with the baseline and NO inhalation groups. We conclude that NO inhaled at 40 ppm has no apparent bronchodilatory effect in pediatric subjects with asthma and mild airways disease. The clinical application of this gas as a therapeutic modality under these conditions is questionable.

The effect of an increase in respiratory dead space on the ventilation during exercise was studied in 4 normal subjects breathing through a mixing chamber of variable volume at one or more work loads. The resulting increases in ventilation and alveolar Pco₂ were dependent on the work load and the volume of added dead space. The magnitude of the changes were related to the subject’s ventilatory response to CO₂, as measured at rest. The level of exercise, CO₂ output, or volume of dead space did not appear to have independent effects on the ventilatory response.

Increasing doses of histamine, 0.00025-0.001 mg of the phosphate/kg body weight, were given intravenously to five normal subjects, seven asthmatics and five chronic bronchitics. Changes in specific airway conductance (SGaw) were measured with a body plethysmograph.In all groups there was significant depression of SGaw following injection of all three doses of histamine but no group was significantly different from another.It is concluded that bronchial reactivity to intravenous injection of histamine does not provide a diagnostic test for separating chronic bronchitis from asthmatics.

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