Nasopulmonary bronchomotor reflexes elicited by mechanical or irritant stimulation of the nose have been described in animals and asthmatic patients. However, few studies were devoted to the consequences of nasal breathing of cold and dry air or of only dry or only moist air on the bronchomotor control in normal individuals. The present study reported changes in interruption resistance (Rint) measured during eupneic breathing of moderately cold (-4 or -10 degrees C) and dry [0.3% relative humidity (RH)] air or of room air at 23 degrees C that is either dry (0.3% RH) or moist (97% RH). Nasal inhalation of cold (-4 degrees C) dry air or of only dry air significantly increased baseline Rint value (17 and 21%, respectively) throughout the 15-min test periods. The response to cold was significantly accentuated when the air temperature was lowered to -10 degrees C (42%). After nasal anesthesia or inhalation of a cholinergic antagonist, cold air did not induce a change in Rint. Nasal inhalation of moist room air had no effect. No Rint changes were measured during oral breathing of the three test agents. It is concluded that the activation of cold receptors or osmoreceptors in the nasal mucosa induces protective bronchoconstrictor responses in normal individuals.

These results confirm that elite divers present a potentiation of the well-known apnoea response in both SA and DA conditions. This response is associated with higher brain perfusion which may partly explain the high levels of world apnoea records.

During the 7.1-MPa hydrogen-helium-oxygen record human dive, we tested the hypothesis that the increased ambient pressure would alter the maximal muscle performance, specifically that breathing dense gas would lead to fatigue of the respiratory muscle. A group of hand muscles (adductor pollicis, AP) and the inspiratory muscles (IM) were studied in three professional divers. Maximal voluntary contractions (MVC) of AP and maximal inspiratory pressure (P(i(max))) generated by IM were measured prior to the dive, during compression and decompression, and then 1 and 2 months after the dive. The decrease in MVC (-22%) was significant at 3.1 MPa, i.e. at the beginning of the introduction of hydrogen into the breathing mixture, whereas P(i(max)) fell progressively during the dive and decompression (maximal DeltaP(i(max)) = -55%), a significant reduction still being measured 1 month after the dive. The altered IM function was attributed to the consequences of long-term ventilatory loading, a condition associated with breathing a dense gas. The transient decrease in MVC of the skeletal muscle would indicate a possible effect of the hyperbaric environment, possibly the high partial pressure of hydrogen, on neuromuscular drive.

The aim of this study was to establish a relationship between bronchial hyperreactivity to carbachol and reflex bronchomotor response to the activation of cold receptors in the nose, and also to examine whether any differences exist between asthmatic patients with or without symptoms of rhinitis. The changes in interrupting resistance (Rint) induced by nasal eupnoeic inhalation of cold (-5°C) dry air were measured in 22 normal subjects and in 18 asthmatic patients (nine of whom had asthma with rhinitis and nine without) with bronchial hyperreactivity to carbachol. In normal individuals, nasal cold air challenge induced a significant increase in Rint (+31%). This was also the case in asthmatic patients (asthma with rhinitis +49%; asthma alone +40%),but the increase was not significantly larger than for normal individuals. The magnitude of Rint increase induced by nasal cold air breathing was correlated with the sensitivity to carbachol (defined as the dose inducing a 50% increase in specific airway conductance (D50)) in asthmatic patients with symptoms of rhinitis. These observations suggest that airway hyperreactivity is associated with enhanced bronchoconstrictor response to the activation of nasal cold receptors, particularly when rhinitis is present. Eur Respir J 1997; 10: 2250-2254 In a previous study in normal individuals [1], we demonstrated the existence of a nasopulmonary bronchoconstrictor reflex in response to nasal inhalation of cold (-5 to -10°C) dry air during eupnoeic breathing. The afferent arm of this reflex was the trigeminal afferents of the nasal mucosa and the efferent arm was the vagus nerve, as demonstrated by the suppression of the airway response to cold air after nasal local anaesthesia or inhalation of an anticholinergic, respectively. In a recent review, MCFADDEN [2] stated that "after lying dormant for several hundred years, the concept of a causal role for upper airway disease in the production of lower airway symptoms re-emerged, taking the new form of a nasobronchial reflex". Observations of a nasopulmonary bronchoconstrictor reflex in humans are often conflicting. SCHUMACHER et al. [3] failed to demonstrate that nasal deposition of allergen or histamine caused a significant decrease in forced expiratory flow rates in subjects with asthma by a reflex mechanism. On the other hand, 5] reported reflex bronchospasm after nasal irritation by silica particles, and YAN and SALOME [6] found that histamine-induced nasal obstruction elicited a fall in forced expiratory volume in one second (FEV1) in subjects with perennial allergic rhinitis and stable asthma. Moreover, nasal cold challenge with freon-propelled aerosol induced a marked increase in oscillatory resistance in asthmatic patients, laryngectomized or not [7].The aim of this study was to explore the nasopulmonary bronchoconstrictor response to cold air in patients who had atopic disease (asthma with or without associated symptoms of rhinitis) and bronchial hyperreactivity to carbachol. The magnitude of their airway respon...

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