MICROVASCULAR EXUDATIVE HYPERRESPONSIVENESS IN HUMAN CORONAVIRUS-INDUCED COMMON COLD

Background - The inflammatory response of the airway microcirculation in rhinitis and asthma may be recorded as luminal entry of plasma macr omolecules (mucosal exudation). This study examines the exudative resp onsiveness of the subepithelial microvessels in subjects with and with out common cold after inoculation with coronavirus. Methods - The airw ay mucosa was exposed to exudative concentrations of histamine (40 and 400 mu g/ml) before and six days after inoculation. To assess whether mucosal penetration of a topically applied agent was altered, nasal a bsorption of chromium-51 labelled ethylene diamine tetraacetic acid (C r-51-EDTA, MW 372) was also examined. A nasal pool technique kept the challenge and tracer solutes in contact with the same ipsilateral muco sal surface. Concentrations of albumin in lavage fluids were measured as an index of mucosal exudation of plasma. Nasal absorption of Cr-51- EDTA was determined by the cumulated 24 hour urinary excretion of radi oactivity. Results - Nine subjects developed common cold after coronav irus inoculation and 10 remained healthy. Histamine produced concentra tion dependent mucosal exudation of plasma in all subjects before and after coronavirus inoculation. In subjects with common cold, however, the histamine-induced mucosal exudation was significantly augmented co mpared with the group without common cold. This exudative hyperrespons iveness is not explained by an increased baseline exudation because th e lavage regimen used produced comparably low baseline exudation in bo th groups of subjects, nor is it explained by an increased penetration of topical histamine because the ability of the nasal mucosa to absor b Cr-51-EDTA was not significantly increased in the subjects with comm on cold. Conclusions - An increased proclivity of the airway subepithe lial microcirculation to respond with plasma exudation develops during coronavirus-induced common cold. This specific exudative hyperrespons iveness may be a feature of inflammatory airway diseases.