Lee L Y, Kou Y R, Fang L B, Frazier D T
Department of Physiology and Biophysics, University of Kentucky, Lexington.
Respir Physiol. 1992 Apr-May;88(1-2):181-92. doi: 10.1016/0034-5687(92)90039-y.
Inhalation of cigarette smoke has been shown to induce bronchoconstriction which should stimulate slowly adapting pulmonary stretch receptors (PSRs). To test this possibility, the activity of PSRs was recorded from fine afferent filaments of the vagus nerve before and after 120 ml of smoke generated from high-nicotine cigarettes was delivered into the lungs in a single breath in anesthetized, open-chest and artificially ventilated dogs. The base-line activity of PSRs did not change during the first two breaths following smoke delivery. However, PSR activity started to increase by the third breath (post-smoke), concomitant with an increase in tracheal (transpulmonary) pressure. Both the smoke-induced increase in tracheal pressure and the delayed effect on PSRs were prevented by a pretreatment with aerosolized isoproterenol, a bronchodilator, suggesting that the delayed response of PSRs to smoke was elicited by the change in bronchomotor tone. Although smoke evoked a delayed stimulation in the majority (61%) of the PSRs studied, it caused a mild delayed inhibition (24%) or had no effect (15%) in some of the receptors. The variable responses to smoke among PSRs are probably related to the smoke-induced heterogeneous changes of mechanical properties in the lungs and their different anatomic locations.
