Elevation of the nasal mucosal surface temperature after warming of the feet occurs via a neural reflex.

OBJECTIVE: To evaluate in humans the mechanisms underlying the increase in nasal mucosal temperature following immersion of the feet in warm water (42 degrees C). MATERIAL AND METHODS: The nasal mucosal temperature of subjects was measured whilst their feet were immersed in warm water. RESULTS: The nasal mucosal temperature rose quickly on immersion and dissipated equally fast on removal of the feet from warm water. Intranasal lidocaine raised the mucosal temperature slightly after application, but also blocked the feet warming-induced increase in nasal mucosal temperature, suggesting a neural reflex. Whereas the cutaneous-nasal reflex stimulates a transient parasympathetic response, acetylcholine does not seem to contribute to the more prolonged increase in nasal mucosal temperature following immersion of the feet in warm water. Warming of the feet probably leads to a loss of alpha-sympathetic activity of nasal blood vessels and an increase in nasal mucosal temperature because application of phenoxybenzamine, an alpha-sympathetic blocking agent, to the nasal mucosa increased the nasal mucosal temperature. CONCLUSIONS: Our data suggest that the increase in nasal mucosal temperature after warming of the feet is mediated by a neural reflex, which is caused by loss of sympathetic activity of the nasal vasculature and a possible additional contribution of a long-acting parasympathetic mediator.

Effects of intranasal azelastine on the response to nasal allergen challenge.

OBJECTIVES/HYPOTHESIS: Azelastine, a second-generation H1-receptor antagonist, is available for topical administration. The aim of the study was to evaluate the effects of topical intranasal azelastine on the early-phase and the late-phase allergic responses and on nasal hyper-responsiveness to methacholine. STUDY DESIGN: Double-blind, placebo-controlled, two-way crossover study in 20 subjects with seasonal allergic rhinitis, out of their allergy season. METHODS: Subjects were randomly assigned to receive either placebo or two puffs of azelastine twice a day (548 microg/d) for 2 weeks followed by nasal challenge with allergen. Twenty-four hours later, while still receiving treatment, subjects underwent a nasal lavage and a nasal challenge with methacholine. End points included symptom scores, levels of mediators and number of eosinophils in nasal lavages, and the weight of secretions after methacholine challenge. RESULTS: Compared with placebo, treatment with intranasal azelastine resulted in significant reductions in allergen-induced sneezing, rhinorrhea, itching, nasal congestion, and levels of albumin during the early-phase response (P <.05). Azelastine had no effect on levels of histamine or tryptase during the early-phase response. There was a significant eosinophil influx 24 hours after challenge, which was not inhibited by azelastine. Treatment with azelastine had no effect on the levels of albumin, interleukin-4, interleukin-5, intercellular adhesion molecule-1, tumor necrosis factor-alpha, and eosinophil cationic protein during the late-phase response. However, azelastine did show a significant inhibitory effect on the methacholine response 24 hours after nasal allergen challenge (P <.05). CONCLUSIONS: The effects of intranasal azelastine are similar to those of oral second-generation antihistamines.