Publications

Nine asthmatic subjects exercised at low, moderate, and high work rates on a cycle ergometer while breathing filtered, humidified air with or without 0.5 ppm of sulfur dioxide (SO2) in a double-blind study. Subjects first performed these experiments breathing through a mouthpiece while wearing a noseclip (oral breathing) and then repeated the experiments breathing through a facemask that separated and permitted independent measurement of oral and nasal air flow (oronasal breathing). We determined specific airway resistance before and after exercise by body plethysmography. Inhaled by mouthpiece, 0.5 ppm So2 caused bronchoconstriction at moderate and high but not at low work rates. There was a dose-response relationship between the work rate performed and the degree of bronchoconstriction induced. Inhaled oronasally, 0.5 ppm SO2 caused bronchoconstriction only at the high work rate. These findings demonstrate that So2-induced bronchoconstriction is dependent on the work rate of exercise during exposure, that oronasal breathing is only partially effective in preventing the bronchoconstriction observed with oral breathing, and that oronasal breathing is less effective in preventing bronchoconstriction with high than with moderate exercise at this concentration of SO2.

To determine antihistaminic versus anticholinergic effects of atropine in airway smooth muscle, we used an in vitro preparation of canine trachealis muscle strips and determined atropine's effect on contractile responses induced by histamine or by electrical field stimulation of cholinergic nerves. In the first series of experiments, 53 strips had initial responses to field stimulation determined and were then randomly assigned to a control group or to a group treated with atropine before field stimulation was repeated and histamine was given. Atropine in concentrations of 10(-8), 10(-7), and 10(-6) M decreased the response to field stimulation to 61.4, 10.5, and 0% of the initial response, respectively, but had no effect on the responses to histamine. In the second series of experiments, 24 strips were treated with indomethacin to prevent histamine tachyphylaxis; these strips had initial responses to both field stimulation and histamine determined and were then assigned to a control group or to a group treated with atropine before field stimulation and histamine were repeated. In these experiments, a concentration of atropine (10(-6) M), which again completely blocked the response to field stimulation, still had no effect on histamine-induced contraction. We conclude that atropine in a concentration that completely blocks the response to cholinergic nerve stimulation has no antihistaminic effect.