To investigate the mechanisms involved in increasing bronchial reactivity, we made a model of airway reactivity increase in dogs after Type C influenza virus infection. Five beagle dogs were inoculated intranasally with the virus, and the time courses of changes in the hemagglutination inhibition (HI) antibody titer and the bronchial reactivity were determined. To assess bronchial reactivity the dogs were anesthetized, and dose-response curves of pulmonary resistance were obtained against increasing concentrations of acetylcholine aerosol. The dogs infected with the virus showed mild symptoms of rhinorrhea and cough. The HI antibody titer was significantly increased in all dogs, with peak values at 1 to 3 wk after infection. The bronchial reactivity to acetylcholine began to increase towards Day 3, reached a peak at 1 to 2 wk, and returned to a normal level at 4 wk. The airway reactivity to acetylcholine at 2 wk after infection was increased by 2.3 to 6.5 times the normal value in terms of the acetylcholine provocative concentration. The mean increase was significant at 1 wk (p < 0.05), 2 wk (p < 0.01), and 3 wk (p < 0.05). Although both the HI antibody titer and the airway responsiveness increased together towards 1 to 2 wk, no close relationship between these factors was observed thereafter. The present dog model of airway hyperreactivity may be useful for further investigation of the mechanism governing increase in bronchial reactivity with respiratory viral infection in normal subjects as well as in patients with asthma.
|Number of pages||5|
|Journal||American Review of Respiratory Disease|
|Publication status||Published - 1986|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine