Impact of elevated pulmonary blood flow and capillary pressure on lung responsiveness

Abstract

Since alterations in pulmonary hemodynamics may lead to airway hyperreactivity, the consequences of individual changes in pulmonary blood flow (Q̇p) and capillary pressure (Pc) on lung responsiveness were investigated. During maintenance of a steady-state Pc of 5, 10, or 15 mmHg ( groups 1–3), acute increases of Q̇p were generated in isolated, perfused rat lungs by simultaneous pulmonary arterial pressure elevation and venous pressure lowering. Conversely, at constant low ( groups 4 and 5) or high Q̇p ( groups 6 and 7), Pc was lowered or elevated by changing, in parallel, the pulmonary arterial and venous pressures. Pulmonary input impedance was measured under baseline conditions and during methacholine provocation (2–18 μg·kg−1·min−1), whereas the pulmonary hemodynamics were altered in accordance with the group allocation. The airway resistance and constant-phase parenchymal model parameters were identified from the pulmonary input impedance spectra. Increases of Q̇p at constant Pc had no effect on the basal lung mechanics, whereas they enhanced the lung reactivity to methacholine, particularly when high Pc was maintained [peak airway resistance increases of 299 ± 99% (SE) vs. 609 ± 217% at Q̇p levels of 5 and 10 ml/min, respectively, P < 0.05]. In contrast, the change of Pc at constant Q̇p slightly deteriorated the basal parenchymal mechanics without affecting the lung responsiveness. These findings suggest that increases in Q̇p per se may lead to the development of airway hyperreactivity. This phenomenon may contribute to the airway susceptibility under conditions associated with simultaneous elevations in pulmonary vascular pressures and Q̇p, such as exercise-induced asthma and the situation in children with congenital heart diseases.