Like asthma, chronic obstructive pulmonary disease (COPD) is a chronic dise
ase, the most prominent symptom of which is airway obstruction. Airway infl
ammation may be pathogenomic in both diseases, but only in COPD does inflam
mation predominate as a determinant of symptoms to make obstruction largely
refractory to treatment. Despite a more limited degree of reversibility th
an in asthma, beta(2)-agonists are used extensively to reduce airway obstru
ction and to achieve symptomatic improvement, with racemic albuterol being
widely favored. In asthma, bronchodilation and bronchoprotection largely ac
count for symptomatic benefit. In COPD, the capacity of racemic albuterol t
o ameliorate these symptoms is more limited and suppression of edema and of
infiltration and activation of leukocytes acquire greater significance, Du
ring regular use of racemic albuterol in asthma, bronchoprotection diminish
es progressively as hyperresponsiveness becomes increasingly pronounced, a
process that is associated with an infiltration and activation of eosinophi
ls. These paradoxic effects of racemic albuterol may be attributed to pharm
acologic actions of the distomer, (S)-albuterol, As would be expected, homo
chiral (R)-albuterol (levalbuterol) is more potent and effective in asthma
and may have significant advantages if used in COPD, A substantial (4-8-fol
d) reduction in the dose of levalbuterol anticipates lesser side effects an
d diminished risk in patients with cardiovascular disease, Additionally, th
e increased potency and duration of bronchodilation observed in asthma may
extend to COPD, Finally, removal of the proinflammatory actions of (S)-albu
terol may eliminate the persisting obstruction and decrease elastance that
are associated with enhanced inflammation and may allow levalbuterol to sup
press edema and diminish leukocyte activation more effectively.