A Aiirrwwaayy b blloooodd ffllooww a anndd b brroonncchhoovvaassccuullaarr c coonnggeessttiioonn iinn s shheeeepp

Vascular congestion could play an important role in causing airway narrowing in asthma. However, the effects of altered bronchial vascular volume and blood flow on airway morphology and pulmonary resistance have not been studied. The aim of this study was to measure airway calibre and vascular volume during inhalation of reputed dilators and constrictors of the airway vasculature in sheep. After baseline measurements of pulmonary resistance (RL) and airway blood flow (Qaw), anaesthetized 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 mg·ml-1 (n=5). RL and Qaw were measured at the time of peak bronchoconstriction, and the sheep were rapidly killed and lung blood loss prevented. Right lung Qaw was calculated and left lung processed for histology; measurements of cartilaginous airway size, wall thickness and fraction of the wall occupied by blood were made using morphomet- ric techniques. Results showed that 20-30% of the airway wall was occupied by blood 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 hist- amine is contraction of the smooth muscle, and the bronchovascular congestion con- tributes little to airway narrowing in cartilaginous airways of sheep. In addition inhaled alpha-agonists do not constrict the bronchial microvasculature under base- line conditions. Therefore, our results do not support the hypothesis that protec- tion against bronchoconstriction provided by alpha-agonists is due to vasoconstriction.