inquiry objectives: To determine the import of cessation of exposure to pollen onward airway responsiveness to adenosine 5'-monophosphate (AMP) in controls with pollen-induced rhinitis.

inquiry objectives: To determine the import of cessation of exposure to pollen onward airway responsiveness to adenosine 5'-monophosphate (AMP) in controls with pollen-induced rhinitis, and to explore the relationship between changes in airway responsiveness and changes in exhaled nitric oxide (ENO) levels

investigation design: Subjects were studied during the pollen season and public of season.

Setting: Specialist allergy unit in a university hospital.

Patients: Fourteen enthralls without asthma with pollen-induced rhinitis who showed bronchoconstriction in answer to methacholine and AMP during the pollen season and 10 healthy nonatopic manage subjects.

Measurements and results: In subdues with pollen-induced rhinitis, ENO concentrations, provocative concentration of agonist causing a 20% fall in FE[Vsub1] (P[Csub20]) methacholine, and P[Csub20] AMP were determined during the pollen season and gone out of season. Healthy control subdues were studied during the pollen season. In subdues with allergic rhinitis, P[C.sub.20] AMP increased from a geometric mean of 794 mg/mL (95% confidence interval [CI], 316 to 1995 mg/mL) during the pollen season to 3162 mg/mL (95% CI, 1585 to 4000 mg/mL) on the outside of season (p = 0004) The ENO concentrations decreased from 631 parts by billion (ppb) [95% CI, 501 to 794 ppb] during the pollen season to 302 ppb (95% CI, 234 to 380 ppb) not at home of season (p < 0001) The ENO concentrations gone out of pollen season were still significantly increased in bring under rules with pollen-induced rhinitis when compared with healthy sway subjects. There was no relationship between individual changes in ENO evens and changes in either P[Csub20] methacholine or P[Csub20] AMP.

Conclusions: In pollen-sensitive make subordinates with allergic rhinitis, the cessation of aspect to pollen is associated with a significant reduction of airway responsiveness to inhaled AMP. However, no association was place between allergen-induced changes in ENO values and in airway responsiveness to either direct or indirect bronchoconstrictors. These findings remind of that modifications in ENO and in airway responsiveness are the result of different alterations induced through allergen exposure on the lower airways.

explanation words: adenosine 5'-monophosphate; airway responsiveness; allergen exposure; allergic rhinitis; methacholine; nitric oxide

Abbreviations: AMP = adenosine 5'-monophosphate; CI = confidence interval; ENO = exhaled nitric oxide; NO = nitric oxide; P[Csub20] = provocative concentration of agonist causing a 20% fall in FE[Vsub1]; ppb = parts by billion

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Airway hyperresponsiveness, an abnormal increase in airflow limitation after position to a number of nonsensitizing bronchoconstrictive stimuli, is not absent in almost all patients with clinically rife asthma. Clinically and for research ends airway responsiveness (1) is measured from bronchial challenge, usually with methacholine or histamine. (1) the couple agonists act on the relevant receptors onward airway smooth muscle, stimulating airway muscle contraction directly. In contrast, adenosine 5'-monophosphate (AMP) acts indirectly, causing primed mast small room degranulation and the release of proinflammatory mediators (histamine and leukotrienes) with later smooth-muscle contraction. (2-4)

Nitric oxide (NO) is raised in exhaled air from controls with asthma compared with healthy repress subjects, and several studies (56) strenuously suggest that exhaled NO (ENO) measurements think airway inflammation. Different technical factors can have significant weights on absolute values of ENO, on the other hand efforts have been made to standardize measurement processs (7)

Some authors refer to that allergic rhinitis and asthma are manifestations of the same disease in sum of two units parts of the respiratory tract. (8) In support of this hypothesis are the observations that the couple airway diseases share the same turns of increasing incidence, (9) predisposing factors, (10) and pathophysiologic mechanisms. (1112) Furthermore, multiple investigations (113) have shown that more [i]or[/i] less patients with allergic rhinitis on the contrary no history of asthma exhibit airway hyperresponsiveness to direct bronchoconstrictor agents (histamine or methacholine). In addition, a certain quantity of reports have indicated that, in enslaves without asthma and with allergic rhinitis, the mien of airway hyperresponsiveness to inhaled methacholine is associated with increased ENO plains (14) Besides methacholine, an important proportion of make submissives with allergic rhinitis also have increased sensitivity to inhaled AMP. (1516) Because bronchoconstriction induced on AMP depends, at least in part, onward the state of activation of airway mast lonely dwellings (2-4) the bronchial response to AMP may be a more direct marker of allergic airway inflammation than direct bronchoconstrictors in the same state [i]or[/i] condition as histamine or methacholine.

There is convincing evidence that, in sensitized enthralls with pollen-induced rhinitis, natural frontage to pollen during the season call forths an increase in methacholine responsiveness (1718) and also induces inflammatory changes in the lower airways.19 In addition, airway responsiveness to inhaled AMP increases during periods of natural allergen exposing in subjects with asthma, (20) moreover no information is available for enslaves with allergic rhinitis.

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