1. This study was devised to test the hypothesis that dyspnoea could be mediated by unmyelinated vagal sensory nerve endings (type J receptors) situated at alveolar level in the lung.
2. A modified jet nebulizer was used to generate an aerosol of local anaesthetic in particles small enough to allow alveolar deposition. Lignocaine (2% and 5%) produced aerosols with an arithmetic mean diameter (+sd) of 1.5+0.3 and 1.2+0.6 μm respectively, the mass median diameters being 1.7 (geometric standard deviation = 1.2) and 2.5 (geometric standard deviation = 1.7) μm respectively.
3. In experimental animal models a vagally mediated tachypnoea may be induced acutely by pulmonary microembolism. This response is known to be mediated by unmyelinated pulmonary afferent nerves in the vagus. Local anaesthetic agents administered as small particles, but not as large particles, obtunded this response, which suggests that the aerosol was capable of penetration to alveolar level.
4. Upon this background, a clinical study was designed to compare the effects of lignocaine with placebo both given as small-particle aerosols. Six patients, including two with diffuse alveolar pathology and four with chronic airflow obstruction, were studied. Respiratory frequency was determined before and after the aerosol, and exercise tolerance and breathlessness were measured with a 6 min walking test and visual analogue scales.
5. After lignocaine there was no clinical evidence of anaesthesia of the upper airways but bronchoconstriction occurred. While no overall effect of lignocaine on dyspnoea was apparent, individual patients showed some evidence of benefit. Although other factors deserve consideration, the lack of a dramatic effect on dyspnoea suggests that dyspnoea in such patients is not mediated principally by J receptors.