Abstract
BackgroundIn experimental conditions alveolar fluid clearance is controlled by alveolar β2-adrenergic receptors. We hypothesized that if this occurs in humans, then non-selective β-blockers should reduce the membrane diffusing capacity (DM), an index of lung interstitial fluid homeostasis. Moreover, we wondered whether this effect is potentiated by saline solution infusion, an intervention expected to cause interstitial lung edema. Since fluid retention within the lungs might trigger excessive ventilation during exercise, we also hypothesized that after the β2-blockade ventilation increased in excess to CO2 output and this was further enhanced by interstitial edema.Methods and Results22 healthy males took part in the study. On day 1, spirometry, lung diffusion for carbon monoxide (DLCO) including its subcomponents DM and capillary volume (VCap), and cardiopulmonary exercise test were performed. On day 2, these tests were repeated after rapid 25 ml/kg saline infusion. Then, in random order 11 subjects were assigned to oral treatment with Carvedilol (CARV) and 11 to Bisoprolol (BISOPR). When heart rate fell at least by 10 beats·min−1, the tests were repeated before (day 3) and after saline infusion (day 4). CARV but not BISOPR, decreased DM (−13±7%, p = 0.001) and increased VCap (+20±22%, p = 0.016) and VE/VCO2 slope (+12±8%, p<0.01). These changes further increased after saline: −18±13% for DM (p<0.01), +44±28% for VCap (p<0.001), and +20±10% for VE/VCO2 slope (p<0.001).ConclusionsThese findings support the hypothesis that in humans in vivo the β2-alveolar receptors contribute to control alveolar fluid clearance and that interstitial lung fluid may trigger exercise hyperventilation.
Highlights
During acute fluid overload, gas exchange in the lungs is preserved as a result of at least two major mechanisms
These findings support the hypothesis that in humans in vivo the b2-alveolar receptors contribute to control alveolar fluid clearance and that interstitial lung fluid may trigger exercise hyperventilation
Under these conditions, reduced DLCO and/or DM have been consistently reported to be associated to a reduced exercise capacity [13,14], reduced ventilatory efficiency [15] and poor prognosis [16]. b-blockers are among the cornerstone tools for heart failure (HF) treatment [17,18] but substantial functional differences have been documented within this class of medications
Summary
Gas exchange in the lungs is preserved as a result of at least two major mechanisms. In heart failure (HF), gradual accumulation of fluid across the lungs leads to a decrease of gas exchange capacity [13] presumably when fluid accumulation in the interstitial space and reabsorption by alveolar Na+ transport systems are fully exploited. Under these conditions, reduced DLCO and/or DM have been consistently reported to be associated to a reduced exercise capacity [13,14], reduced ventilatory efficiency [15] and poor prognosis [16]. Since fluid retention within the lungs might trigger excessive ventilation during exercise, we hypothesized that after the b2-blockade ventilation increased in excess to CO2 output and this was further enhanced by interstitial edema
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