Am. J. Respir. Crit. Care Med., Vol 151, No. 3, 03 1995, 830-835.
Acetylcholine release from airway cholinergic nerves in horses with heaves, an airway obstructive disease
ZW Wang, MF Yu, NE Robinson and FJ Derksen
Pulmonary Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing.
The present study was conducted to determine if acetylcholine (ACh) release
from airway cholinergic nerves is increased and if modulation of ACh
release by prejunctional receptors is altered in horses with heaves, an
obstructive airway disease characterized by airway inflammation and
bronchospasm. Trachealis strips and bronchial segments of normal horses and
horses affected with heaves were suspended in 2-ml tissue baths. ACh
release was induced by electrical field stimulation and the bath ACh
content was measured by high performance liquid chromatography (HPLC) with
electrochemical detection. In response to electrical field stimulation, the
rate of ACh release from cholinergic nerves innervating the trachea was not
significantly different between the two groups of horses. The nonselective
muscarinic receptor antagonist atropine augmented ACh release to the same
extent in both groups, indicating that there is no dysfunction of
muscarinic autoreceptors on cholinergic nerves of large airways from horses
with heaves. Compared with the data from normal horses, the inhibitory
effect of the alpha 2-adrenoceptor agonist clonidine on ACh release was
lacking in the bronchi and less potent in the trachea, suggesting that the
prejunctional alpha 2-adrenoceptors are dysfunctional in horses with
heaves. Neither exogenous prostaglandin E2 (PGE2) nor the cyclooxygenase
inhibitor indomethacin influenced ACh release from the bronchi, suggesting
that a decrease in airway mucosal PGE2 production reported previously in
horses with heaves does not alter ACh release.
