1. Eight mongrel dogs were studied to evaluate the effect of local inflammation on the response of collateral airways to histamine. In each dog we measured the baseline collateral resistance and its response to increasing doses of nebulized histamine. These measurements were obtained at weekly intervals, twice under control conditions and in three subsequent weeks after a local instillation of the bacteria Bordetella bronchiseptica. On each study day, after the measurements of collateral resistance, we lavaged the studied lung segment by instilling and aspirating 100 ml of saline (four 25 ml aliquots). All studies were performed in the same lung segment.
2. Collateral resistance remained stable under control conditions at 19.5 ± 7.2 and 11.7 ± 32 cm H2OI−l mm. With a bacteria-induced, mostly neutrophilic, inflammation, collateral resistance initially increased to 70.2 ± 18.6 cm H2OI−1 min after 1 week and subsequently decreased towards control values (47.3 ± 13 and 30.7 ± 10.1 cm H2OI−1 min at 21 and 29 days, respectively). Collateral pathways reactivity, expressed as the slope of the relationship collateral resistance/log (1 + [histamine]), remained unchanged throughout the study. The values of this slope were (mean ± SEM) 0.021 ± 0.003 and 0.022 ± 0.004 in the two control studies and 0.025 ± 0.004, 0.030 ± 0.006 and 0.023 ± 0.003 in the three subsequent weekly studies. Inflammation, evaluated by the number of bronchoalveolar lavage cells and the percentage of neutrophils in bronchoalveolar cells, closely paralleled baseline collateral resistance with a peak value at the first week after the infection.
3. Local inflammation increases collateral resistance by its mechanical effects, and does not modify the responsiveness of collateral pathways to nebulized histamine.