Present evidence suggests that chronic obstructive pulmonary disease (COPD) of horses is a delayed hypersensitivity response to inhaled antigens, particularly the thermophilic moulds and actinomycetes that grow in damp hay. Within several hours of exposing COPD-susceptible horses to such hay, neutrophils invade the lung and accumulate in the lumens of airways, particularly bronchioles. The inflammatory response is accompanied by increased levels of histamine in bronchoalveolar lavage fluid, increased plasma levels of the inflammatory mediators thromboxane and 15-hydroxyeicosatetraenoic acid (15-HETE), and a decrease in the production of prostaglandin (PG) E2 by the airway mucosa. During acute exacerbations of COPD, airways exhibit nonspecific hyperresponsiveness and become obstructed as a result of bronchospasm and the accumulation of mucus and exudates. Bronchospasm is due largely to activation of smooth muscle muscarinic receptors by acetylcholine (ACh). Because the in vitro response of smooth muscle to ACh is unaltered, the increase in airway smooth muscle tone is probably a result of activation of airway reflexes by inflammatory mediators and decreases in inhibitory mechanisms such as the intrapulmonary nonadrenergic noncholinergic nervous system and the production of PGE2 in affected horses. The diffuse airway obstruction leads to uneven distribution of ventilation, ventilation/ perfusion mismatching, and hypoxaemia. As a result of the increased respiratory drive caused by hypoxaemia and the presence of airway obstruction, horses adopt a characteristic breathing strategy in which very high peak flows at the start of exhalation rapidly diminish as exhalation proceeds.
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