Rationale: Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction. Objectives: This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves. Methods: Specific airway resistance (SR aw ) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49 8 C; HA) and room temperature (20-22 8 C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients. Measurements and Main Results: SR aw increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SR aw by only 22% in healthy subjects; there was no difference between their SR aw responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma. Conclusions: Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.Keywords: asthma; cough; bronchoconstriction; TRPV1; ipratropium It is extensively documented that breathing cold dry air induces bronchoconstriction in patients with asthma, which results primarily from injury of airway mucosa and release of various bronchoactive autacoids, such as leukotrienes and histamine (1). In contrast, the effects of an increase in temperature on the airway functions in patients with asthma is generally overlooked despite the fact that hyperthermia occurs frequently under normal and pathophysiological conditions. The most common causes of hyperthermia are elevated metabolic rate (e.g., during exercise) and hindered heat dissipation (e.g., in a warm environment). Hyperthermia can also occur under disease conditions, such as in patients suffering from severe fever. Furthermore, tissue inflammation is known to lead to local hyperemia and an increase in tissue temperature in the inflamed area (2, 3). A recent study has reported that the average end-expiratory temperature plateau (as an indirect measurement of the lung tissue temperature) is 2.7 8 C higher in children with asthma than that in healthy control subjects (4).An earlier study by Aitken and Marini ...

We studied the respiratory responses to an increase in airway temperature in patients with allergic rhinitis (AR). Responses to isocapnic hyperventilation (40% of maximal voluntary ventilation) for 4 minutes of humidified hot air (HA; 49 °C) and room air (RA: 21 °C) were compared between AR patients (n=7) and healthy subjects (n=6). In AR patients, cough frequency increased pronouncedly from 0.10±0.07 before to 2.37±0.73 during, and 1.80±0.79 coughs/min for the first 8 minutes after the HA challenge, but not during the RA challenge. In contrast, neither HA nor RA had any significant tussive effect in healthy subjects. The HA challenge also caused respiratory discomfort (mainly throat irritation) measured by the handgrip dynamometry in AR patients, but not in healthy subjects. Bronchoconstriction was not detected after the HA challenge in either group of subjects. In conclusion, hyperventilation of HA triggered vigorous cough response and throat irritation in AR patients, indicating the involvement of sensory nerves innervating upper airways.

Finger tremor and extrapyramidal side-effects (EPSEs) were measured in seven patients before and during neuroleptic drug treatment to assess the relationship between the onset of EPSEs and changes in finger tremor spectra. Tremor and EPSEs were also measured in twelve patients stabilized on neuroleptic drugs to determine whether tremor could provide a reliable index of the presence and severity of extrapyramidal system disturbance. A downward shift in peak tremor frequently was noted within 48 hours of starting neuroleptic drug therapy, usually before the onset of EPSEs, and a significant negative relationship between the severity of EPSEs and tremor frequency (but not tremor amplitude). The peak frequency of finger tremor is thus a sensitive index of extrapyramidal disturbance and might be of value in predicting which patients taking neuroleptic drugs need anti-parkinsonian therapy.

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