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Oxymetazoline nasal spray three times daily for four weeks in normal subjects is not associated with rebound congestion or tachyphylaxis.

Topical decongestants are available over the counter and provide rapid relief of nasal obstruction for conditions of short duration, for example the common cold. Manufacturers' recommendations are that topical decongestants should not be used regularly for more than 1 week in view of the risk of rebound mucosal hyperaemia with persistent nasal obstruction and refractoriness to further effects of decongestants. For this reason we performed a randomised double-blind placebo-controlled trial in 30 normal adult subjects with 0.05% oxymetazoline nasal spray 2 sprays (0.1 ml/spray) to each nostril 3 times daily over an extended period of 4 weeks. Degree of nasal blockage was assessed before and after 4 weeks treatment and for 2 weeks following discontinuation of treatment. Outcome measures included diary symptom scores and measurements of nasal peak inspiratory flow, airway resistance (using posterior active rhinomanometry) and volume (using acoustic rhinometry). Nasal patency was assessed at baseline and 15 minutes after oxymetazoline challenge at each clinic visit. Results demonstrated no significant increases in subjective nasal blockage throughout the 6 weeks study period in either oxymetazoline- or placebo-treated subjects. No significant differences were observed between groups for baseline measurements of nasal peak inspiratory flow, airway resistance or volume at each clinic visit. A highly significant decongestant effect of oxymetazoline was observed at each clinic visit with changes in all 3 measurements for both treatment groups, again with no significant differences between groups. In summary, in normal subjects, we identified no significant nasal blockage or impaired decongestant response to oxymetazoline following 4 weeks treatment with oxymetazoline compared to matched placebo nasal spray.

Administration, Intranasal↗

Tachyphylaxis.

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Humans↗

[Effect on beta adrenergic receptors of tachyphylaxis on the sensitivity of smooth muscle in the bronchi to beta adrenergic receptor agonists in bronchial asthma].

The study involved 30 subjects: 15 healthy individuals and 15 patients with atopic bronchial asthma of the moderate degree. Salbutamol was administered to asthmatic patients in the intravenous infusion for 7 days. beta-adrenergic receptor density in the lymphocytes and FEV1 were evaluated before and after therapy. Moreover, isoprenaline test was carried out to evaluate the sensitivity of the bronchial smooth muscle to beta-agonist. The test was performed prior to and after salbutamol therapy. It was found that beta-receptor agonist statistically significantly decreases beta-adrenergic receptor density. Equivalently, bronchial smooth muscle is less sensitive to beta-agonist in the same degree as a decrease in beta-adrenergic receptor density in the peripheral blood lymphocytes.

Adolescent↗

[Tachyphylaxis induced by repeated inhalation of bradykinin in asthmatic patients].

Bradykinin is a nonapeptide, which may act as a mediator in asthma since it is generated upon nasal immunological challenge in vivo and it has been shown to induce some asthma-like symptoms. In vitro studies suggest that refractoriness following bradykinin challenge may be due to release of contractile tachykinins. In this study it was shown that repeated bronchial challenge with bradykinin in atopic asthmatic subjects induced loss of response to the nonapeptide. Once achieved, reduced bradykinin responsiveness was not accompanied by loss of airways response to histamine. Moreover, repeated challenge with histamine failed to produce a significant loss of airways response to this agonist. In conclusion, either the depletion of contractile tachykinins or the down-regulation at the level of specific kinin receptors might account for the refractoriness following repeated inhalation of bradykinin in asthmatic subjects.

Adult↗

[Tachyphylaxis].

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Animals↗