Bronchial Hyperresponsiveness to Inhaled Methacholine in Subjects with Chronic Left Heart Failure at a Time of Exacerbation and After Increasing Diuretic Therapy

Interactions between pulmonary hemodynamics and lung mechanics

“…The previous studies, however,were conducted under clinical settings on a wide variety of patients as concerns the type, the severity and the history of the respiratory and circulatory disease, factors which may bias an evaluation of the lung responsiveness. Our study, conducted under well-controlled conditions, confirms the occurrence of BHR in the presence of left-heart failure [3][4][5]8], with the additional information that the airways display an enhanced reactivity to a constrictor agonist (serotonin) that is not acting on the cholinergic receptors directly. The changes in the Raw following serotonin challenges demonstrate the presence of a dose-dependent airway constriction, while the increases in G exceeding those in H are likely to be a consequence of severe ventilation heterogeneities [46].…”

“…However, a reduction of the left ventricular preload by diuretics, leading to a partial clearance of the edema fluid, had no effects on the baseline lung mechanics and responsiveness [4], suggesting that the pulmonary consequences of left heart failure cannot be fully explained on a geometric basis or by fluid accumulation around the airways. Besides these mechanisms, the development of interstitial edema may uncouple the airways from the lung parenchyma by altering the mechanical interdependence between the airways and the surrounding lung tissue [29].…”

“…Understanding the relationships between the pulmonary vasculature and bronchoalveolar networks has major importance in pathophysiological conditions encountered in various cardiopulmonary diseases, such as coronary ischaemia leading to left heart failure [3][4][5], congenital heart malfunctions [6,7] or valvular disfunction [5,8].…”

“…Some authors demonstrated the induction of bronchial hyperresponsiveness (BHR) to lung provocations [3][4][5]8] whereas others found no evidence of BHR in patients with chronic congestive heart failure [24,25]. In addition to this controversy, the underlying pathophysiological mechanisms leading to airway narrowing and occasionally BHR after pulmonary lung congestion have not been completely clarified.…”

“…In addition, serotonin increases release of acetylcholine thereby enhancing the cholinergic tone of the airway smooth muscle. Previous studies on patients with left-heart failure yielded inconsistent conclusions regarding the presence or absence of BHR, with a majority of the papers reporting airway hyper-responsiveness to exogenous cholinergic constrictor stimuli [3][4][5]8], whereas others described a normal airway reactivity [24,25]. The previous studies, however,were conducted under clinical settings on a wide variety of patients as concerns the type, the severity and the history of the respiratory and circulatory disease, factors which may bias an evaluation of the lung responsiveness.…”