Alpha 1-adrenergic-induced airway obstruction in ponies with recurrent pulmonary disease

We examined the response of five ponies with recurrent airway obstruction (principals) and five age- and gender-matched controls to the aerosol alpha-adrenergic agonist phenylephrine after blockade with propranolol and atropine. Measurements were made with principal ponies in clinical remission (period A) and during acute airway obstruction (period B). The blockade had no effect on base-line pulmonary mechanics in control ponies during periods A and B or in the principal ponies during period A. However, in the principal ponies during period B, blockade increased dynamic compliance (Cdyn) and decreased pulmonary resistance (RL). Phenylephrine had no effect on the controls during either period. In the principals, phenylephrine decreased Cdyn and increased RL during both periods. The alpha 1-agonist aerosol prazosin shifted the phenylephrine dose-response curves to the right, but prasozin did not bronchodilate the principals during period B. This suggests that the role of alpha 1-adrenergic receptors in airway narrowing in ponies with recurrent airway obstruction is minimal. However, the response to phenylephrine in only the principal ponies suggests an increase in alpha-receptor numbers and/or activity in these animals compared with controls.     

Effects of atropine in ponies with recurrent airway obstruction

The effects of atropine on lung function and airway reactivity in two groups of ponies were measured. Principal ponies had a history of recurrent airway obstruction when housed in a barn and fed hay; control ponies had no history of airway obstruction. Principal and control ponies were paired, and measurements were made when principal ponies were in clinical remission (period A) and during an acute attack of airway obstruction (period B). Atropine did not alter pulmonary resistance (RL), dynamic compliance (Cdyn), or airway responsiveness in either group of ponies at period A or in the controls at period B. In principal ponies at period B, atropine did not alter Cdyn or the concentration of aerosol histamine required to decrease Cdyn to 65% of base line (ED65Cdyn) but reduced RL and the change in RL induced by 0.1 mg/ml histamine (delta RL0.1). It is likely that the latter observation was due to geometric changes in the airways, because the change in RL and in delta RL0.1 were significantly correlated. The results of this study show little resting bronchomotor tone in normal ponies, but a major portion of the increase in RL in principals at period B is mediated via muscarinic receptors. Little evidence exists for muscarinic receptor involvement in the response to aerosol histamine in either principal or control ponies.     

Beta-adrenergic blockade in ponies with recurrent obstructive pulmonary disease

Ponies with recurrent airway obstruction have hyperresponsive airways during acute disease exacerbations but not during clinical remission. We examined the effect of beta-adrenergic blockade with propranolol on airway responsiveness to aerosol histamine in six ponies with recurrent airway obstruction and six age- and gender-matched controls. Measurements were made with principal ponies in clinical remission (period A) and during an acute period of airway obstruction (period B). beta-Adrenergic blockade did not change airway responsiveness, dynamic compliance (Cdyn), or pulmonary resistance (RL) in either group of ponies at period A or in the control ponies at period B. In principal ponies at period B, propranolol significantly increased RL but was without effect on Cdyn or airway responsiveness. We conclude that the beta-adrenergic system is involved in the control of central airway caliber in principal ponies at period B but that this system does not seem to be involved in the mechanism of airway hyperresponsiveness to histamine.