In this study active anterior (AAR) and active posterior (APR) rhinomanometry were performed by 100 normal subjects with a Mercury rhinomanometer according to the recommendations of the International Standardization Committee. There was no significant difference between total nasal airway resistance (Rna) values obtained with APR by direct measurement and those calculated from AAR. Mean total Rna was 0.31 Pa/cm3/s (range 0.13-0.84) at a reference pressure of 75 Pa. Measurements by AAR were more reproducible than those by APR, mean intrasubject coefficients of variation were 12 and 16% respectively. This reproducibility was similar to that of lower airways' resistance measurements. Rna values from this population did not conform to a normal Gaussian distribution. Rna was higher during expiration than inspiration and values were higher in women than in men.

The aim of this study was to determine the role of histamine receptors in the nose. The effects of intranasal histamine challenge were compared with those of a specific H1-receptor agonist, betahistine and a specific H2-receptor agonist, impromidine, in 11 normal individuals and four with rhinitis. Sneezing, nasal irritation and hypersecretion were induced by histamine and the H1-receptor agonist, betahistine only. Nasal airway resistance (Rna) was measured by passive anterior rhinomanometry. Histamine, betahistine and impromidine all induced rises in Rna in both normal individuals and those with rhinitis but histamine had the most potent effect; the H2-receptor effect on Rna was predominant over that of the H1-receptor. The sensitivity to all three agonists was greater in the individuals with rhinitis.

Two established methods (active posterior and passive anterior rhinomanometry) and 2 new methods (peak nasal inspiratory flow rate and apparent nasal volume) were used in 12 volunteers to assess the patency of the nasal airways under each of 4 conditions (baseline, post-exercise, nasal histamine and nasal cocaine). All methods showed the congestant effect of histamine but the peak nasal inspiratory flow and apparent nasal volume techniques were more sensitive to the 'decongesting' manoeuvres, (exercise and cocaine). Useful objective quantitative data on the patency of the nasal airways and its changes in response to stimuli can be obtained by simple, cheap and readily available techniques. Subjective sensation is a poor guide to the state of patency of the nasal airways.

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The permeability of respiratory mucosa, as measured by clearance of diethylenetriamine penta-acetate (DTPA) labelled with technetium 99m, was similar in seven normal and nine asthmatic subjects. Histamine induced bronchoconstriction was associated with a 50% increase in permeability in both groups of subjects. In normal subjects inhaled salbutamol, given as 1 mg acutely or as 200 ,ug four times daily for two weeks, had no effect on pulmonary permeability. Salbutamol, given before histamine challenge, prevented bronchoconstriction, but did not affect the increase in permeability seen in normal subjects. Low doses of histamine, sufficient to cause bronchoconstriction in the asthmatic subjects, produced little bronchoconstriction in normal subjects but caused increases in lung permeability similar to those seen in asthmatic subjects. These studies suggest that these two effects of inhaled histamine, bronchoconstriction and increased permeability, are independent.

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