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

Marco Guazzi, Roberto Brambilla, Piergiuseppe Agostoni, Maurizio D. Guazzi

Research output: Contribution to journalArticle

Abstract

Aims: In congestive heart failure (CHF), pulmonary gas exchange, as evaluated by carbon monoxide diffusion (DLCO), is impaired. ACE-inhibition improves DLCO. Infusion of saline worsens DLCO, because of upregulated sodium and water transport to the alveolar interstitium, which thickens the alveolar-capillary interface and lengthens the diffusion path for gas exchange. We investigated whether enalapril can readjust the capillary permeability to sodium. Methods: In 10 NYHA class II-III CHF patients, we measured DLCO, its two subcomponents (VC, 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 baseline and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily). Results: Saline (150 ml) significantly reduced DLCO (-9.1%) and DM (-9.8%) and augmented VC (+10.7%). Responses to 750 ml saline were somewhat greater and qualitatively similar. Enalapril produced a significant improvement of DLCO and DM at rest as well as after saline, that was not associated with variations in ventricular filling pressures, cardiac output and left ventricular ejection fraction, and was not accounted for by humoral changes. Conclusions: In CHF, ACE-inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium.

Original languageEnglish
Pages (from-to)482-487
Number of pages6
JournalBritish Journal of Clinical Pharmacology
Volume51
Issue number5
DOIs
Publication statusPublished - 2001

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Pulmonary Gas Exchange
Enalapril
Heart Failure
Salts
Gases
Sodium
Ventricular Pressure
Lung
Capillary Permeability
Carbon Monoxide
Blood Volume
Aldosterone
Renin
Cardiac Output
Stroke Volume
Pulmonary Artery
Endothelium
Norepinephrine
Membranes
Water

Keywords

  • Enalapril
  • Heart failure
  • Pulmonary function

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Influence of ACE-inhibition on salt-mediated worsening of pulmonary gas exchange in heart failure. / Guazzi, Marco; Brambilla, Roberto; Agostoni, Piergiuseppe; Guazzi, Maurizio D.

In: British Journal of Clinical Pharmacology, Vol. 51, No. 5, 2001, p. 482-487.

Research output: Contribution to journalArticle

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abstract = "Aims: In congestive heart failure (CHF), pulmonary gas exchange, as evaluated by carbon monoxide diffusion (DLCO), is impaired. ACE-inhibition improves DLCO. Infusion of saline worsens DLCO, because of upregulated sodium and water transport to the alveolar interstitium, which thickens the alveolar-capillary interface and lengthens the diffusion path for gas exchange. We investigated whether enalapril can readjust the capillary permeability to sodium. Methods: In 10 NYHA class II-III CHF patients, we measured DLCO, its two subcomponents (VC, 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 baseline and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily). Results: Saline (150 ml) significantly reduced DLCO (-9.1{\%}) and DM (-9.8{\%}) and augmented VC (+10.7{\%}). Responses to 750 ml saline were somewhat greater and qualitatively similar. Enalapril produced a significant improvement of DLCO and DM at rest as well as after saline, that was not associated with variations in ventricular filling pressures, cardiac output and left ventricular ejection fraction, and was not accounted for by humoral changes. Conclusions: In CHF, ACE-inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium.",
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N2 - Aims: In congestive heart failure (CHF), pulmonary gas exchange, as evaluated by carbon monoxide diffusion (DLCO), is impaired. ACE-inhibition improves DLCO. Infusion of saline worsens DLCO, because of upregulated sodium and water transport to the alveolar interstitium, which thickens the alveolar-capillary interface and lengthens the diffusion path for gas exchange. We investigated whether enalapril can readjust the capillary permeability to sodium. Methods: In 10 NYHA class II-III CHF patients, we measured DLCO, its two subcomponents (VC, 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 baseline and following saline infusion in the main pulmonary artery stem, before and after 1 week enalapril treatment (20 mg daily). Results: Saline (150 ml) significantly reduced DLCO (-9.1%) and DM (-9.8%) and augmented VC (+10.7%). Responses to 750 ml saline were somewhat greater and qualitatively similar. Enalapril produced a significant improvement of DLCO and DM at rest as well as after saline, that was not associated with variations in ventricular filling pressures, cardiac output and left ventricular ejection fraction, and was not accounted for by humoral changes. Conclusions: In CHF, ACE-inhibition attenuates the deterioration of pulmonary gas transfer produced by saline infusion, suggesting an ability to readjust the upregulated sodium transport across the pulmonary microvascular endothelium.

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