Asbestos in Lung Cancer

important structures for conditioning luminal gas temperature and humidity. Functionally, nasal vasculature resemble bronchial vasculature in their response to environmental, physical, chemical, nervous and humoral stimuli. M i have extensively studied several factors which regulate nasal airflow resistance(Rnaw)and nasal blood flow(Qn)in man, including nasal or oral hyperventilation and physical exercise.3 if bronchial blood vessels react similar to nasal blood vessels (as we believe), rebound bronchial vascular congestion (RBrC) 5 to 10 mm postexercise could explain the hypothesis suggested by McFadden’ and Gilbert et al in the pathogenesis ofat least the early phase of EIA. Nasal blood vessels in patients with allergic rhinitis (with or without bronchial asthma) are hyperplastic and hypertrophied; so are bronchial blood vessels in patients with bronchial asthma. The response ofthese blood vessels to various stimuli is also exaggerated. The usual response of physical exercise in both healthy subjects and patients with allergic rhinitis (with or without bronchial asthma) is an immediate decrease in Rnaw due to an increase in sympathetic nervous activity, causing vasconstriction of the precapillary and capacitance vessels in the nose.3 This response is initiated in the hypothalamus. The prompt decrease in Rnaw is followed by a recovery phase, which is faster in patients with allergic rhinitis with bronchial asthma, especially in those who develop EIA.3 In about 60 percent ofpatients with allergic rhinitis and bronchial asthma there is a pronounced rebound in Rnaw which is due to rebound nasal vascular congestion (RNC). This occurs 5 mm postexercise in patients who develop EIA; at the same time, these patients begin to experience symptoms of exercise-induced bronchoconstriction. If bronchial blood vessels reacted similar to nasal blood vessels during and following exercise, there would be vasoconstriction of bronchial precapillary and capacitance vessels, all aimed at conserving expiratory heat and water loss. This could be followed by rebound bronchial vascular congestion (RBrC) similar to RNC a few minutes after exercise. Rebound bronchial vascular congestion could itself lead to bronchial mucosal edema and swelling, hyposmolarity of bronchial mucosa which could trigger mediator release and promote postexercise-induced bronchoconstriction. The mechanisms underlying RNC and RBrC in patients with allergic rhinitis and bronchial asthma are less clear but this response is consistent with a high degree of vascular and mucosal lability in these patients.