Summary
Pulmonary function measurements were made in control ponies and in ponies with recurrent obstructive pulmonary disease (principals) during clinical remission and during an attack of acute airway obstruction. The ponies were given β-adrenergic antagonists and agonists to determine the role of β receptors in recurrent obstructive pulmonary disease, and to determine the subtypes of β receptors mediating bronchodilation in ponies. Aerosol administration of the β antagonists, propranolol (β1 and β2), atenolol (β1), and butoxamine (β2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Intravenous administration of atropine reversed the effect of atenolol on Cdyn and RL, but was without effect on the decrease in Cdyn and increase in RL observed after butoxamine administration. The β antagonists did not affect airway function in the control ponies. The effect of β blockade on Cdyn and RL suggests β-adrenergic activation in the central and peripheral airways of principal ponies, mediated through both β2- and β1-adrenergic receptors. The aerosol β agonists, isoproterenol (β1 and β2), and clenbuterol (β2) attenuated histamine-induced airway obstruction to a similar extent in control ponies that were given histamine iv. In addition, the β1 antagonist, atenolol, did not attenuate the bronchodilation observed with isoproterenol. We concluded that, although β1- and β2-adrenergic receptors exist in pony airways and are activated during acute airway obstruction, bronchodilation in response to β agonists in ponies seems to be mediated primarily by β2-adrenergic receptors.
