Influence of ACE-inhibition on salt-mediated worsening of pulmonary gas exchange in heart failure

Citation
M. Guazzi et al., Influence of ACE-inhibition on salt-mediated worsening of pulmonary gas exchange in heart failure, BR J CL PH, 51(5), 2001, pp. 482-487
Citations number
17
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY
ISSN journal
03065251 → ACNP
Volume
51
Issue
5
Year of publication
2001
Pages
482 - 487
Database
ISI
SICI code
0306-5251(200105)51:5<482:IOAOSW>2.0.ZU;2-8
Abstract
Aims In congestive heart failure (CHF), pulmonary gas exchange, as evaluate d by carbon monoxide diffusion (DLCO), is impaired. ACE-inhibition improves DLCO. Infusion of saline worsens DLCO, because of upregulated sodium and w ater transport to the alveolar interstitium, which thickens the alveolar-ca pillary interface and lengthens the diffusion path for gas exchange. We inv estigated whether enalapril can readjust the capillary permeability to sodi um. Methods In 10 NYHA class II-III CHF patients, we measured DLCO, its two sub components (V-C, capillary blood volume available for gas exchange, and DM, alveolar-capillary membrane diffusion), left and right ventricular filling pressures, plasma noradrenaline, aldosterone and renin activity, at baseli ne and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily). Results Saline (150 mi) significantly reduced DLCO (-9.1%) and D-M (-9.8%) and augmented V-C (+10.7%). Responses to 750 mi saline were somewhat greate r and qualitatively similar. Enalapril produced a significant improvement o f DLCO and D-M at rest as well as after saline, that was not associated wit h variations in ventricular filling pressures, cardiac output and left vent ricular ejection fraction, and was not accounted for by humoral changes. Conclusions In CHF, ACE-inhibition attenuates the deterioration of pulmonar y gas transfer produced by saline infusion, suggesting an ability to readju st the upregulated sodium transport across the pulmonary microvascular endo thelium.