Effect of Airway Blood Flow on Airflow

Abstract

Resistance to gas flow of an airway is a function of both airway smooth muscle tone and thickness of the airway wall internal to the outer ring of airway smooth muscle. Schematically, the increase in airway resistance caused by shortening of airway smooth muscle may be potentiated by a concomitant increase in airway wall thickness caused by vasodilation of the bronchial vessels and/or microvascular leakage. Conversely, bronchial vasoconstriction may limit to some extent the increase in resistance to gas flow caused by airway smooth muscle shortening and/or congestion and edema of the airway wall. Many endogenous paracrine mediators, putatively involved in asthma and bronchial hyperresponsiveness, have both bronchomotor and vascular effects. The overall effects on resistance to airflow of endogenous or exogenous agents depend not only upon pre-existing airway smooth muscle tone and pre-existing condition of bronchial vessels but also upon two factors that facilitate microvascular leakage, namely, inflammation of the airway wall and outflow pressure of the bronchial circulation, which is close to left atrial pressure.

Influence of bronchial blood flow and conductance on pulmonary function in stable systolic heart failure

“…However the results of several studies provide indirect evidence that changes in bronchovascular conductance may be related to changes in pulmonary function and symptoms of congestion in HF (Cabanes et al 1992; Lockhart et al 1992; Wetzel et al 1993; Agostoni et al 1995; McIlveen 2000). In an early study of anesthetized mini-pigs, Wetzel and colleagues (1993) demonstrated that intravascular volume loading resulted in bronchial mucosal engorgement and decreased airway cross sectional area.…”

Interactions between pulmonary hemodynamics and lung mechanics

“…Some authors have suggested that, after the administration of cholinergic agonists with vasodilator properties, bronchial vasodilation plays a major role by distorting the airway geometry [3,8,61]. However, we observed BHR to a bronchoactive agent with a pulmonary vasoconstrictor potential, thus this mechanism was not involved in the enhanced responsiveness of the airways.…”

Muscarinic receptors involved in airway vascular leakage induced by experimental gastro-oesophageal reflux

“…The role of M 1 and M 3 receptors in airway plasma extravasation is of potential clinical interest since resistance to gas flow of an airway is a function of both airway smooth muscle tone and thickness of the airway wall internal to the outer ring of airway smooth muscle. Schematically, the increase in airway resistance caused by shortening of airway smooth muscle may be potentiated by a concomitant increase in airway wall thickness caused by vasodilatation of the bronchial vessels and/or microvascular leakage (Lockhart et al, 1992).…”