The influence of pulmonary receptors on respiratory drive in a rabbit model of pulmonary emphysema.

We have observed that pulmonary rapidly adapting receptor activity is greater in emphysematous rats than in controls. Pulmonary receptor activity, if modified by lung disease, may produce an inappropriate drive to breathe which may be perceived as dyspnoea. To investigate the efferent (drive) component of this hypothesis respiratory drive (phrenic nerve activity) was recorded in a rabbit model of emphysema. Drive was measured as slope and peak height of phrenic nerve activity. Slope and peak height were greater in emphysematous rabbits than controls, by 28% and 34%, respectively. Block of slowly adapting pulmonary stretch receptors by inhaled sulphur dioxide (which left only rapidly adapting and C-fibre receptors active) decreased drive in control (slope: 38.89+/-2.29 to 24.09+/-1.26, P<0.01) but not emphysematous rabbits (slope: 49.92+/-4.11 to 54.51+/-5.28, NS). Subsequent vagotomy decreased drive in emphysematous rabbits (slope: 54.51+/-5.28 to 41.41+/-3.90, P<0.05) but not controls (24.09+/-1.26 to 23.07+/-1.84, NS). Increased rapidly adapting receptor activity may, in part, increase respiratory drive in emphysema. This vagal component is only part of the total increased drive which may be perceived as dyspnoea in man.