Airway Heat and Water Exchange

Abstract

Hyperventilation of dry or cool air causes respiratory heat and water loss, and elicits airflow obstruction in patients with exercise-induced asthma. Though the mechanism by which heat and/or water fluxes are transduced to local airway narrowing remains uncertain, considerable insight has been gained. Theoretical and experimental analyses of intra-airway heat and water transfers have demonstrated that: (1) increasing minute ventilation (MV) promotes further penetration of cool, dry, inspired gas into the lung before it has been fully warmed and humidified to alveolar gas conditions; (2) lowering inspired gas temperature or humidity at fixed MV increases local heat/water losses, but the axial distribution of those losses remains largely unchanged; (3) the net change in airway wall temperature or hydration depends importantly upon the effectiveness of local heat and water replenishing sources that resist the airway cooling and dessication promoted by local heat/water losses. Experimentally documented sequelae of dry gas hyperpnea include broncho-constriction (found in the central airways of guinea pigs and of human asthmatic subjects, and in the dog lung periphery), broncho-vascular arterial dilatation (confirmed in dogs and sheep, and possibly in normal humans), and broncho-vascular hyperpermeability (demonstrated in guinea pigs and ferrets). One or several facets of the physical events that accompany dry gas hyperpnea lead to the release of bronchoactive and vasoactive mediators (including eicosanoids and tachykinins, from animal studies) that could conceivably provoke airflow obstruction by direct stimulation of airway smooth muscle, or by promoting broncho-vascular engorgement and/or hyperpermeability, with consequent edema formation.

Supported by NHLBI Grants HL02205 and HL41009.