Lung congestion augments the responses of cells in the rapidly adapting receptor pathway to cigarette smoke in rabbit.

1. We examined the effects of cigarette smoke, inhaled alone and during mild pulmonary venous congestion, on the activity of fifty-three neurones in the nucleus tractus solitarii (NTS) that were excited by input from pulmonary rapidly adapting receptors (RAR). Ten neurones excited by slowly adapting stretch receptors (SAR) were also studied. 2. Extracellular recordings of RAR-activated neurones were recorded in alpha-chloralose anaesthetized rabbits. Smoke from low- and high-nicotine cigarettes was delivered through a ventilator. Mild pulmonary venous congestion was produced by inflating a balloon in the left atrium. 3. Inhalation of three breaths of smoke from low-nicotine cigarettes increased the activity of fifty-one out of fifty-three RAR-activated neurones from 5.9 +/- 1.0 to 14.4 +/- 2.1 spikes breath-1 (P < 0.05). 4. The responses of fifteen neurones were compared with smoke inhaled alone or during mild pulmonary venous congestion. Smoke alone increased unit activity from 6.8 +/- 2.3 to 12.6 +/- 3.7 spikes breath-1 (P < 0.05). Small increases in left atrial pressure (2.0 +/- 0.5 mmHg) had no effect on baseline unit activity (7.6 +/- 2.11 vs. 7.7 +/- 2.3 spikes breath-1; P > 0.05), but enhanced the responses to smoke, increasing the activity from 7.6 +/- 2.1 to 17.1 +/- 4.8 spikes breath-1 (P < 0.05). The response was greater than to smoke alone (P < 0.05). 5. Of ten SAR-activated neurones, seven failed to respond to inhaled cigarette smoke, two were excited and one was inhibited. Pulmonary venous congestion had no effect on the unit activity before and after smoke (n = 4 neurones). 6. We conclude that smoke-evoked excitation of RAR lower-order neurones is augmented by pulmonary venous congestion.