Cigarette smoke acutely increases collateral resistance in excised dog lobes.

The acute effects of cigarette smoke or drug inhalation on collateral conductance (Gcoll) were studied in freshly excised dog lobes held at fixed volumes. A double-lumen catheter was wedged into a segmental bronchus, and air, smoke, or aerosol flowed into the blocked segment at a constant pressure of 2 cmH2O. A capsule glued over a small area of perforated pleura of the segment was used to measure alveolar pressure; the capsule could also be used to measure small airway flow (Vcap) through the segment. Gcoll was almost linearly dependent on lung volume, rising about fivefold between 20 and 100% inflation (30 cmH2O). During smoke inhalation Gcoll began decreasing almost immediately, roughly halving with the first cigarette and falling to about 20% after two cigarettes. Similar proportions were obtained at other lung volumes. Pulmonary conductance (oscillator) in the remainder of the lobe decreased only modestly to 78% of control after two cigarettes. In lobes exposed to 4.5% CO2 after air Gcoll rose 25-50%, but Vcap increased only 5-10%. However, acetylcholine chloride aerosol reduced both flows by similar ratios. Isoproterenol did not prevent or reverse smoke-induced collateral constriction but did reverse the effects of acetylcholine on both pathways. These results suggest that in excised lungs aerosols acted on larger segmental airways in series with collateral channels and with peripheral airways, whereas CO2 and particularly cigarette smoke provoked more marked effects on the most distal smooth muscle.