Publications

Exercise and the resultant hyperpnea increase the magnitude of many stimuli delivered to the airways. Thus clinical "exercise-induced" bronchoconstriction can probably be initiated by a number of stimuli including, for example, sulfur dioxide, which is present in polluted air. In the laboratory, when subjects perform exercise breathing clean air, the water content of the inspired air is a major determinant of the bronchoconstriction induced, whereas in our hands, the temperature of the inspired air is of little or no importance, even over a range associated with significant differences in airway cooling. These observations support the view that water loss is an important stimulus to exercise-induced bronchoconstriction, perhaps as a result of a transient increase in the osmolarity of airway surface liquid.

Previous work by Bloedow et al. evaluated the effect of warfarin on diltiazem binding. Unbound diltiazem remained constant (22.5 +/- 3.6 per cent) in the presence of warfarin. We studied 10 patients, 51 to 72 years old, who were receiving warfarin as an anticoagulant for valvular replacement, thrombosis, or embolus. Our study demonstrates that a single 120-mg oral diltiazem dose, sufficient to cause hemodynamic changes, does not displace warfarin from plasma binding sites.