Bronchial responsiveness to inhaled histamine in canine pulmonary congestion

To elucidate the role of bronchial hyperresponsiveness (BHR) in pulmonary congestion, an inhaled histamine provocation test was performed in dogs with acute pulmonary congestion, and the role of vagal nerve activity and arachidonic acid metabolites on bronchial responsiveness was evaluated. We assessed BHR with the provocation concentration of histamine causing a 100% increase in pulmonary resistance (PC100) in an openchest anesthetized and tracheotomized canine model before and after left atrial balloon inflation. Twenty-two mongrel dogs (8-14 kg) were anesthetized with sodium thiopental (15-20 mg/kg) and mechanically ventilated with positive end-expiratory pressure at 3 cmH2O. A Foley catheter was inserted into the left atrium to cause pulmonary congestion, in which mean left atrial pressure was increased to 18 mmHg. In 6 dogs, histamine provocation was examined before and after pulmonary congestion was effected. Intravenous indomethacin (1 mg/kg) administration and vagotomy were performed in 5 dogs. In pulmonary congestion, PC100 was significantly decreased both before and after vagotomy and after indomethacin administration. We conclude that pulmonary congestion augments bronchial responsiveness to inhaled histamine and that neither vagotomy nor indomethacin administration prevents bronchial hyperresponsiveness in pulmonary congestion. These findings suggest that bronchial hyperresponsiveness in pulmonary congestion is related to another factor such as bronchial edema.