Modification of bronchial blood flow during allergic airway responses

Ascaris suum antigen effects on mean airflow resistance (RL) and bronchial arterial blood flow (Q̇br) were studied in allergic anesthetized sheep with documented airway responses. Q̇br was measured with electromagnetic flow probes, and supplemental O₂ prevented antigen-induced hypoxemia. Aerosol challenge with this specific antigen increased RL and Q̇br significantly. Cromolyn sodium aerosol pretreatment prevented antigen-induced increases in RL but not in Q̇br. Intravenous cromoly, however, prevented increases in Q̇br and RL, suggesting a role for mast cell degranulation in both bronchomotor and bronchovascular responses to antigen. Antigen-induced increases in Q̇br were not solely attributable to histamine release. Indomethacin pretreatment attenuated the antigen-induced increase in Q̇br, thus suggesting that vasodilator cyclooxygenase products contribute to the vascular response. Antigen challenge significantly decreased Q̇br after indomethacin and metiamide pretreatment, which suggests that vasoconstrictor substances released after antigen exposure also modulate Q̇br; however, released vasodilators overshadow vasoconstrictor effects. Thus antigen challenge affects Q̇br by locally releasing histamine and vasodilator prostaglandins as well as vasoconstrictor substances. These effects were independent of antigen-induced changes in systemic and pulmonary hemodynamics.