AIRWAY BLOOD-FLOW AND BRONCHOVASCULAR CONGESTION IN SHEEP

Vascular congestion could play an important role in causing airway nar rowing in asthma. However, the effects of altered bronchial vascular v olume and blood flow on airway morphology and pulmonary resistance hav e not been studied. The aim of this study was to measure airway calibr e and vascular volume during inhalation of reputed dilators and constr ictors of the airway vasculature in sheep. After baseline measurements of pulmonary resistance (RL) and airway blood flow (Qaw), anaesthetiz ed sheep inhaled an aerosol of either: 0.9% saline (n=6); histamine 16 mg.ml-1 (n=5); phenylephrine 0.1-10 mg.ml-1 (n=6), or methoxamine 1 m g.ml-1 (n=5). RL and Qaw were measured at the time of peak bronchocons triction, and the sheep were rapidly killed and lung blood loss preven ted. Right lung Qaw was calculated and left lung processed for histolo gy; measurements of cartilaginous airway size, wall thickness and frac tion of the wall occupied by blood were made using morphometric techni ques. Results showed that 20-30% of the airway wall was occupied by bl ood vessels. Inhalation of histamine caused an increase in Qaw and RL, and a 50% increase in the vascular volume fraction of the airway wall , whereas inhaled alpha-agonists did not reduce Qaw or vascular volume fraction. We conclude that the major cause of airway narrowing after inhalation of histamine is contraction of the smooth muscle, and the b ronchovascular congestion contributes little to airway narrowing in ca rtilaginous airways of sheep. In addition inhaled alpha-agonists do no t constrict the bronchial microvasculature under baseline conditions. Therefore, our results do not support the hypothesis that protection a gainst bronchoconstriction provided by alpha-agonists is due to vasoco nstriction.