Study of the pulmonary circulation in a canine asthma model.

Measurements of respiratory mechanics, gas exchange, and pulmonary hemodynamics were made before and serially for 2 hours after inhalation challenge with Ascaris suum extract in dogs with natural sensitivity to this antigen. Nine of 14 dogs randomly exposed to an inspired oxygen fraction of 0.21 or 0.60 to 0.70, responded to the challenge with bronchospasm reflected by a transient decrease of mean specific respiratory system conductance to 50 per cent of baseline after 5 to 15 min. This was accompanied by a decrease in alveolar ventilation in all and acidosis in some animals. No changes were observed in transmural pulmonary arterial pressure, cardiac output, pulmonary vascular resistance, and pulmonary blood volume in all 9 dogs who responded with bronchospasm, whether or not arterial hypoxemia was allowed to develop. In contrast, a significant increase in pulmonary vascular resistance occurred in control dogs in whom comparable degrees of arterial hypoxemia were produced by 10 per cent oxygen breathing or mechanical bronchial obstruction by placing beads in lobar and segmental airways. No changes in any parameter measured occurred in the 5 dogs who did not develop bronchospasm after antigen challenge. The results indicated that moderately severe, antigen-induced bronchospasm in anesthetized dogs has no effect on the pulmonary circulation even when associated with arterial hypoxemia. Because nonuniformity of alveolar hypoxia allowing redistribution of blood flow is probably not responsible for this failure to develop increases in pulmonary vascular resistance in induced asthma, it is suggested that the elaboration of chemical mediators may have interfered with the hypoxic pulmonary vasoconstrictor response.