Ovalbumin-induced lung disease in the pony: role of vagal mechanisms.

In awake sensitized ponies, we studied the effect of aerosol ovalbumin challenge on ventilation, pulmonary mechanics, lung volume, and gas exchange before and after vagal blockade. We also challenged the left lung and measured respiratory rate (f) and right and left respiratory system resistance (RrsR, RrsL) before and after both left and bilateral vagal section. Bilateral ovalbumin aerosol challenge increased f, minute ventilation (VE), total respiratory system resistance (Rrs), and minimal volume, decreased dynamic compliance, total lung capacity, and arterial oxygen tension, and was without effect on tidal volume (VT), functional residual capacity, quasi-static lung compliance, and arterial carbon dioxide tension. Vagal blockade reversed the increase in f, VE, and Rrs and increased VT. Challenge of the left lung increased f and RrsL but did not alter RrsR. Bilateral vagal section reversed the tachypnea but unilateral section did not. Histopathologic lesions included acute fibrinopurulent obstructive bronchiolitis, bronchitis, edema, and alveolar distension. We conclude that local mechanisms are of critical importance in the pathogenesis of ovalbumin-induced airway obstruction in ponies, that increased sensitivity of airway smooth muscle to normal vagal tone may also play a role, and that tachypnea following challenge is caused by activity of pulmonary receptors with vagal afferent fibers.