Airway Inflammation Affects Airway and Distal Circulatory Control

In the distal airways (small bronchi and alveoli) the gas remains fully saturated with water vapour. At 37°C this 100% relative humidity means a 44mg/L water content or a 47mmHg PH2O. Therefore, the water content of inspired gas is usually lower than in the alveolar gas, and water has to be added to inspired air along the airways. During resting breathing, most of the necessary water vapour is transferred from the mucosa of nose or mouth, which also rewarm the inspired air. However, with high ventilation rates, unconditioned (cold and low-water content) air reaches the larynx, trachea or even segmental bronchi. The inspired airstream is then warmed up and loaded with water vapour (evaporation of mucus water) by the airway wall. Delivering heat and evaporating water levels is performed through an important energy loss by the airway mucosa. This energy loss cools the airway wall (McFadden & Pichurko, 1985), and this cooling is sensed by sensory nerves (Coleridge & Coleridge, 1994; Agostoni et al., 1990; Salonen et al., 1991), which triggers the release of mediators by nerves or inflammatory cells, e.g. histamine by mast cells. The nerve fibre stimulation can also stimulate epithelial cells and increase their production of many paracrine mediators (Jallat-Daloz et al., 2001). In normobaric conditions with air breathing, most of the energy provided by the airway wall to humidify and re-warm the inspired air is required by water vaporisation from the mucus layers (Varène, 1986). The convective heat loss (direct heat exchange) becomes conspicuous only in hyperbaric conditions (high gas density), or when gas with a high specific heat (e.g. helium) is used instead of nitrogen (Varène, 1986; Jammes et al., 1988). It was first described by Gilbert et al. (1987) that airstream temperatures in the airways re-warmed faster in asthmatic than in healthy subjects after the wall cooling caused by hyperventilation of dry air. These authors hypothesised that a larger development of the airway mucosal vascular network and an increased vascular reactivity contributed to this special feature in the asthmatic subjects. The larger development of the airway vasculature in inflammatory conditions has been well documented in animals (McDonald, 1988) and humans (Laitinen & Laitinen, 1990; Li & Wilson, 1997). Continuous measurement of the expired gas temperature confirmed airway rewarming to be faster in asthmatic subjects than in non-asthmatics, and this difference was suppressed when an a-adrenoceptor agonist was inhaled (Regnard et al., 1989). It was also observed that squeezing the legs and thighs of upright subjects through inflation of shock trousers (i.e. the rapid shifting of 150 to 400mL of blood from the lower limbs into the thorax) caused a sudden increase in expired temperatures in asthmatics (Regnard et al., 1989), as well as a rapid increase in tracheal and bronchial airstream temperatures (Gilbert et al., 1991). These results support the idea that the tracheobronchial blood flow was likely to increase to a much larger extent in asthmatic subjects with inflammatory mucosa, than in healthy subjects, even without any acute asthma episode (Valléry-Radot et al., 1950). More recently this larger airway blood flow in asthmatics was evidenced through measurements of dimethylether absorbtion (Kumar et al., 1998). The increase in airway mucosal blood flow triggered in healthy subjects by inhaled b2-agonists was not found in asthmatics (Kumar et al., 1998), but was partly restored SHORT REVIEW